Shikonin is a plant medicine extracted from , which dominate influential antioxidant and antitumor effect. Here, we report that shikonin was capable of inducing human esophageal cancer EC9706 cell apoptosis and autophagy, in a time- and dose-dependent manner. Shikonin exposure repressed cell viability and migration and invasion capabilities and caused EC9706 cell autophagy and apoptosis by activating the AMPK/mTOR/ULK axis. Autophagy inhibition secured EC9706 cells against shikonin-induced autophagy and apoptosis and reversed the upregulation of AMPK and ULK phosphorylation and downregulation of mTOR phosphorylation provoked by shikonin. In summary, shikonin instigates EC9706 cell apoptosis and autophagy using the target AMPK/mTOR/ULK signal pathway axis, which provides a potential new target to treat human esophageal cancer.

Colorectal cancer (CRC) stands as a significant global health issue, marked by elevated occurrence and mortality statistics. Despite the availability of various treatments, including chemotherapy, radiotherapy, and targeted therapy, CRC cells often exhibit resistance to these interventions. As a result, it is imperative to identify the disease at an earlier stage and enhance the response to treatment by acquiring a deeper comprehension of the processes driving tumor formation, aggressiveness, metastasis, and resistance to therapy. The Hippo pathway plays a critical role in facilitating the initiation of tumorigenesis and frequently experiences disruption within CRC because of genetic mutations and modified expression in its fundamental constituents. Targeting upstream regulators or core Hippo pathway components may provide innovative therapeutic strategies for modulating Hippo signaling dysfunction in CRC. To advance novel therapeutic techniques for CRC, it is imperative to grasp the involvement of the Hippo pathway in CRC and its interaction with alternate signaling pathways, noncoding RNAs, gut microbiota, and the immune microenvironment. This review seeks to illuminate the function and control of the Hippo pathway in CRC, ultimately aiming to unearth innovative therapeutic methodologies for addressing this ailment.

Astrocyte proliferation commonly occurs after spinal cord injury (SCI). N-Acetylcysteine (NAC) has a regulatory effect on many diseases. In this study, we investigated the effect and underlying mechanism of NAC on astrocytes in SCI. We isolated rat primary astrocytes and stimulated with lipopolysaccharide to induce cell proliferation and degeneration. A rat model of SCI was also established, and the Basso-Beattie-Bresnahan score was determined. The localization of glial fibrillary acidic protein in the cells and tissues was determined using TUNEL staining and immunofluorescence, while that of connexin 43 was assessed via immunofluorescence. Pathological changes associated with SCI were detected using hematoxylin and eosin staining, and inflammatory factors were detected using enzyme-linked immunosorbent assay. Additionally, JAK/STAT expression was evaluated using western blotting and quantitative reverse transcription polymerase chain reaction. NAC downregulated the glial fibrillary acidic protein abundance and connexin 43 in reactive astrocytes and SCI rat models while inhibiting the abundance of secreted proteins DSPG, HSPG, KSPG, tenascin C, vimentin, CSPG, ephrin-B2, and nestin. NAC also regulated the JAK/STAT signaling pathway by downregulating the expression of JAK2, STAT5, STAT3, STAT1, PIM1, NFATc1, COL1, COL3, TGF-, SMAD1, CTGF, CyCD1, and CDK4, thus alleviating SCI. Finally, NAC exhibited durable effects, with no SCI recurrence within 60 days. Therefore, NAC relieves SCI by inhibiting the proliferation of reactive astrocytes and suppressing the expression of secretory and JAK/STAT pathway proteins.

Mutations in SLC25A32 in humans cause late-onset exercise intolerance, which is associated with various neurological and metabolic diseases. However, its specific mechanism of action in tumour development is poorly understood owing to the lack of multiomics integrated analysis of SLC25A32 in pan-cancer.

Gastric cancer (GC) is the most common malignant tumor and ranks third in the world. LncRNA H19 (H19), one of the members of lncRNA, is overexpressed in various tumors. However, many undetermined molecular mechanisms by which H19 promotes GC progression still need to be further investigated. . A series of experiments was used to confirm the undetermined molecular mechanism including wound healing and transwell assays. . In this study, a significant upregulation of H19 expression was detected in GC cells and tissues. The poor overall survival was observed in GC patient with high H19 expression. Overexpression of H19 promoted the migration of GC cells, while knockdown of H19 significantly inhibited cell migration. Moreover, miR-148a-3p had a certain negative correlation with H19. Luciferase reporter assay confirmed that H19 could directly bind to miR-148a-3p. As expected, miR-148a mimics inhibited cell migration and invasion induced by H19 overexpression. The above findings proved that H19 functions as a miRNA sponge and verified that miR-148a-3p is the H19-associated miRNA in GC. We also confirmed that SOX-12 expression was upregulated in GC patient's samples. SOX-12 expression was positively correlated with expression of H19 and was able to directly bind to miR-148a-3p. Importantly, wound healing assay showed that knockout of SOX-12 could reverse the promoting effect of H19 overexpression on cell migration.

Osteosarcoma (OS), characterized by a complex tumor microenvironment, poses challenges in treatment, metastasis, and therapy resistance. This study examined the impact of lactylation, a posttranslational modification, on gene expression and tumor behavior in OS, particularly its influence on prognosis, immune cell infiltration, and chemotherapy response. Utilizing data from the Gene Expression Omnibus series accession number 21257 (GSE21257) and the Therapeutically Applicable Research to Generate Effective Treatments on Osteosarcoma (TARGET-OS) datasets, the investigation focused on analyzing the expression profiles of 267 lactylation modifier genes, which were selected from a total of 336 lactylation-related genes compiled from various studies in the literature. The methods included unsupervised clustering using "ConsensusClusterPlus" heatmap generation with "pheatmap" pathway analysis from several databases, and immune cell infiltration assessment using the "single-sample Gene Set Enrichment Analysis (ssGSEA)" function. The research revealed 36 significant lactylation-related genes in OS, categorizing them into two clusters with distinct survival and biological characteristics. One cluster demonstrated poor prognosis due to increased tumor cell proliferation and specific immune cell variations, also showcasing genes that enhance tumor growth and metastasis, thus indicating its aggressive nature and adverse outcomes for patients. These insights are crucial for understanding the molecular mechanisms of OS and identifying therapeutic targets. Therefore, the study elucidates the role of lactylation-related genes in the prognosis, pathogenesis, and treatment response of OS, laying the groundwork for further exploration into potential therapeutic targets and the underlying mechanisms within OS.

Fibroblasts play a crucial role in diabetic wound healing, and their senescence is the cause of delayed wound repair. It was reported that fibroblasts can secrete exosomes that can mediate a vital role in diabetic complications. Our purpose is to examine the biological function of high glucose (HG)-induced senescent fibroblasts from the perspective of exosomes and reveal the mechanism at cellular and animal levels. HG-induced senescent fibroblasts were measured by senescence-associated -galactosidase staining and immunofluorescence. Flow cytometry, 5-ethynyl-2'-deoxyuridine (edu), and cell counting kit 8 (CCK-8) assay were applied to detect apoptosis and cell viability. Fibroblasts and endothelial cells were cocultured, and the migration and angiogenesis abilities were detected by scratch, transwell, and tube formation assays. Exosomes were isolated and identified from fibroblasts that were treated differently. Then, the function of exosomes was investigated in cells and mice, including examining the cellular phenotype changes, detecting the autophagy levels, and evaluating the wound healing rate. Furthermore, the potential mechanism by which senescent fibroblast-derived exosomes inhibit wound healing was examined via bioinformatics, real-time quantitive polymerase chain reaction (qPCR), transfection, and dual-luciferase assays. It illustrated that HG-induced senescent fibroblasts exhibited adverse impacts on cellular proliferation, migration, and angiogenesis of endothelial cells via secreting exosomes, and senescent fibroblast-derived exosomes (S-Exos) can delay skin wound defects in mice. Subsequent differential analysis of the GSE153214 and GSE48417 datasets elucidated that miR-497 was the biomarker in the senescent fibroblasts. Interestingly, the miR-497 levels were also elevated in S-Exos. Its overexpression can regulate human umbilical vein endothelial cell function by regulating autophagy via targeting ATG13. Furthermore, experiments also illustrated that miR-497 can delay wound healing and reduce autophagy. Our study demonstrated that exosomes from senescent fibroblasts can impair endothelial cell function and impede diabetic wound healing. The underlying mechanism was that fibroblast-derived exosomal miR-497 can target ATG13 to reduce autophagy, offering insight into new therapy for diabetic complications and other diseases.

Oral squamous cell carcinoma (OSCC) is a prevalent and aggressive form of head and neck cancer, often diagnosed at advanced stages. Elucidating the molecular mechanisms involved in the malignant transformation from normal oral tissue to oral preinvasive lesions (OPL) and primary OSCC could facilitate early diagnosis and improve therapeutic strategies. Differentially expressed genes (DEGs) were identified from the GSE30784 dataset by comparing normal oral tissue, oral dysplasia, and primary OSCC samples. Cross-validation was performed using an independent RNA-seq dataset, GSE186775. Protein-protein interaction (PPI) network analysis, gene ontology annotation, and pathway enrichment analysis were conducted on the common DEGs. Hub genes were identified, and their prognostic significance was evaluated using survival analysis. Transcription factor (TF) enrichment analysis, cross-validation, and immunohistochemistry analyses were also performed. A total of 226 proteins and 677 interactions were identified in the PPI network, with 34 hub genes, including FN1, SERPINE1, PLAUR, THBS1, and ITGA6. Pathways such as "Formation of the cornified envelope," "Keratinization," and "Developmental biology" were enriched. Overexpression of SERPINE1, PLAUR, THBS1, and ITGA6 correlated with poor prognosis, while upregulation of CALML5 and SPINK5 was associated with favorable outcomes. NFIB emerged as the most significant TF-regulating hub genes. Immunohistochemistry validated ITGA6 overexpression in primary OSCC. Cross-validation using the RNA-seq dataset supported the involvement of critical genes in the malignant transformation process. This study identified vital genes, pathways, and prognostic markers involved in the malignant transformation from normal oral tissue to OPL and primary OSCC, providing insights for early diagnosis and targeted therapy development. Cross-validation with an independent RNA-seq dataset and immunohistochemistry reinforced the findings, supporting the robustness of the identified molecular signatures.

DEAD-box helicase 21 (DDX21) is a conserved Asp-Glu-Ala-Asp (DEAD) box RNA helicase with multiple functions that is involved in various cellular processes and diseases. However, the role of DDX21 in the recurrence and prognosis of hepatocellular carcinoma (HCC) patients remains unknown. In the current study, we examined the protein expression of DDX21 in HCC tissues through immunohistochemical staining and analyzed the correlation between DDX21 protein expression and clinical outcome via Kaplan-Meier survival analysis. The Cox proportional hazards regression model was used to assess the interrelationships between the outcome and variable over time. Our results showed that increased expression of DDX21 protein was observed in HCC tissues compared with paracancerous tissues and was associated with advanced BCLC stage. Recurrent HCC patients had higher levels of DDX21 protein than nonrecurrent cases. Notably, DDX21 was an independent risk factor for predicting worse overall survival and recurrence-free survival in HCC patients. Furthermore, lack of DDX21 abated the growth and mobility of Hep3B cells. Taken together, our data highlight the clinical significance of DDX21 in the recurrence and prognosis of HCC patients and indicate that targeting DDX21 may represent an effective therapeutic strategy for the treatment of HCC.

Lung cancer is a highly prevalent and fatal cancer that seriously threatens the safety of people in various regions around the world. Difficulty in early diagnosis and strong drug resistance have always been difficulties in the treatment of lung cancer, so the prognosis of lung cancer has always been the focus of scientific researchers. This study used genotype-tissue expression (GTEx) and the cancer genome atlas (TCGA) databases to obtain 477 lung adenocarcinoma (LUAD) and 347 healthy individuals' samples as research subjects and divided LUAD patients into low-risk and high-risk groups based on prognostic risk scores. Differentially expressed gene (DEG) analysis was performed on 25 pyroptosis-related genes obtained from GeneCards and MSigDB databases in cancer tissues of LUAD patients and noncancerous tissues of healthy individuals, and seven genes were significantly different in cancer tissues and noncancerous tissues among them. Coexpression analysis and differential expression analysis of these genes and long noncoding RNAs (lncRNAs) found that three lncRNAs (AC012615.1, AC099850.3, and AO0001453.2) had significant differences in expression between cancer tissues and noncancerous tissues. We used Cox regression and the least absolute shrinkage sum selection operator (LASSO) regression to construct a prognostic model for LUAD patients with these three pyroptosis-related lncRNAs (pRLs) and analyzed the prognostic value of the pRLs model by the Likaplan-Meier curve and Cox regression. The results show that the risk prediction model has good prediction ability. In addition, we also studied the differences in tumor mutation burden (TMB), tumor immune dysfunction and rejection (TIDE), and immune microenvironment with pRLs risk scores in low-risk and high-risk groups. This study successfully established a LUAD prognostic model based on pRLs, which provides new insights into lncRNA-based LUAD diagnosis and treatment strategies.

Due to the difficulty in early diagnosis and the lack of treatment for advanced disease, the mortality rate of hepatocellular carcinoma (HCC) is high, and the 5-year overall survival rate is low at present. SLC1A4 is a neutral amino acid transporter, but its regulatory role and mechanism in HCC are still unclear. Through analyzing the TCGA database and clinical tissue specimens, this study uncovered the high expression of SLC1A4 in tumor tissues of HCC. Worse more, a high level of SLC1A4 may lead to a poor prognosis of HCC. Mechanically, silencing SLC1A4 inhibited the phosphorylation activation of AKT by suppressing the ubiquitin modification of AKT at lysine 63 and amino acid influx represented by D-serine, decreasing the protein level of -catenin in the cell nucleus and suppressing the transcriptional activity of c-Myc and EpCAM promoters. As a result, silencing SLC1A4 inhibited the proliferation, migration, and stemness of hepatic cancer cells, which was successfully reversed by the introduction of exogenous AKT. Moreover, epithelial-mesenchymal transition (EMT) in vitro and metastasis potential in vivo of hepatic cancer cells was suppressed by the downregulated SLC1A4 level. In conclusion, SLC1A4 promotes the malignant transformation of HCC through activating signal transduction mediated by AKT. The findings in this study suggested that SLC1A4 may be a diagnostic indicator for the early HCC and a therapeutic target for the advanced HCC.

Circular RNA (circRNA) is implicated in various biological processes, including the progression of gastric cancer (GC). The specific functions and underlying mechanisms of circ_0079226 in GC are unknown. We examined cancerous and adjacent noncancerous tissues from 25 patients with GC to evaluate circ_0079226, miR-155-5p, and forkhead transcription factor K1 (FOXK1) expression. Pearson's correlation analysis was used to assess the relationships among these RNAs. We examined their functional roles utilizing in vitro (cell cytotoxicity kit-8, wound healing, and Transwell invasion assays) and in vivo (xenograft mouse models) approaches. Molecular mechanisms were investigated using bioinformatics, dual-luciferase reporter assays, and rescue experiments, while quantitative real-time PCR, western blot, immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), and protein immunofluorescence (IF) were used to detect gene expression. We found that circ_0079226 and FOXK1 levels were elevated, while miR-155-5p was reduced in GC tissues and cells. An inverse correlation existed between FOXK1 and miR-155-5p, while a direct correlation was observed between FOXK1 and circ_0079226. Circ_0079226 facilitated GC cell proliferation, migration, invasion, and in vivo tumor growth. It functions by sequestering miR-155-5p, which directly targets FOXK1. High miR-155-5p expression mitigated the effects of circ_0079226 on GC cells, and the reintroduction of FOXK1 reversed the inhibitory effects of miR-155-5p. Circ_0079226 boosts FOXK1 and its associated downstream signaling pathways, including FAK, AKT, and p-AKT, through competitive binding with miR-155-5p. In conclusion, circ_0079226 is implicated in GC cell proliferation and metastasis by modulating the miR-155-5p/FOXK1/AKT pathway, presenting it as a potential therapeutic target.

Colloid nodules are common and benign thyroid lesions that usually progress slowly and are asymptomatic. It requires follow-up because untreated colloid nodules may develop into malignant tumor. The study aimed to examine the contributions of vitamin D receptor (VDR) expression, VDR/FokI (rs2228570) genotypes, and serum vitamin D level to the susceptibility to colloid nodules. One hundred forty subjects (80 patients and 60 controls) were enrolled and VDR FokI was determined by PCR in formalin fixed paraffin embedded (FFPE) blocks of the patients and blood of controls. Moreover, VDR protein expression was evaluated by immunohistochemistry using specific VDR monoclonal antibody in the tissue sections of patients and serum vitamin D were measured simultaneously using enzyme-linked immunosorbent assay (ELISA). Sixty-two (77.5%) cases showed strong immunoreactivity score (IRS) of cytoplasmic staining. Strong IRS were significantly observed in samples with larger nodule size ( value: 0.0094), multinodules ( value: 0.0054), and carriers of CC genotypes ( value: 0.0034). TT homozygous genotype revealed significantly ( value: 0.029 and odds ratio (OR): 0.11) protective factor for colloid nodules. In addition, nodule size was significantly ( value: 0.016) larger among CC carriers. Moreover, vitamin D level and category were nonsignificantly difference between patients and controls. Our results reveal prominent cytoplasmic VDR expression, suggesting a distinct distribution pattern and offering valuable insights into its potential role in colloid nodules. VDR expression increases with increasing size and number of nodules. Regarding FokI genotypes, TT genotype was less likely to develop colloid nodule. These findings contribute to our understanding of cellular characteristics of this condition and may have implications for future research and clinical management.

Tumor microenvironment (TME) is essential for the development and progression of hepatocellular carcinoma (HCC). Exosomes participate in constructing TME by passing biological information, but the regulatory effect of PDL1 in exosomes on anticancer activity of CD8 T cells in HCC still needs to be further explored. In this study, high level of PDL1 was found in plasma exosomes of HCC patients, which turned out to be significantly associated with the increased number of tumor nodules, the upregulated level of serum AFP, the raised tendency of TNM stage, and the poor prognosis of HCC. The expression of CD8 may be inhibited in HCC that is characterized with high level of PDL1, and the protein level of exosomal PDL1 was determined by intracellular PDL1 abundance. High level of exosomal PDL1 inhibited the proliferation and activation of CD8 T cells, but exhibited limited effect on the proliferation of hepatic cancer cells. Moreover, the growth of tumors formed by hepatic cancer cells Hepa1-6 in C57L mice was significantly promoted by the exosomal PDL1, which might be caused by the inhibitory effect of exosomal PDL1 on CD8 T cells. Thus, exosomal PDL1 promotes the development and progression of HCC through inhibiting the anticancer activity of CD8 T cells. This study provides sights for understanding the oncogenic role of PDL1 and a reasonable explanation for the low efficacy of anti-PD1/PDL1 immunotherapies in HCC.

Circular RNAs (circRNAs), covalently closed single-stranded RNAs, have been implicated in cancer progression. A previous investigation revealed that circ-ZEB1 is expressed abnormally in liver cancer. However, the roles of circ-ZEB1 in non-small cell lung cancer (NSCLC) are unknown. In this study, we used fluorescence in situ hybridization (FISH) and RT-qPCR to study circ-ZEB1 expression in NSCLC cells and tissues. A luciferase reporter assay was performed to validate downstream targets of circ-ZEB1. Transwell migration, 5-ethynyl-20-deoxyuridine (EdU), and cell counting kit-8 (CCK8) assays were performed to assess proliferation and migration. In vivo metastasis and tumorigenesis assays were also performed to investigate circ-ZEB1 functions during NSCLC. Our results showed that circ-ZEB1 expression was increased in NSCLC tissues and cells. circ-ZEB1 downregulation suppressed NSCLC cell proliferation as well as migration in vitro and in vivo. Luciferase data confirmed EIF5A and miR-491-5p as downstream targets of circ-ZEB1. EIF5A overexpression and miR-491-5p suppression reversed NSCLC cell migration post circ-ZEB1 silencing. Our collective findings advised that circ-ZEB1 takes part in the malignant progression through regulating the miR-491-5p/EIF5A axis, highlighting its potential as an effective NSCLC therapeutic target.

As an important downstream effector of various signaling pathways, mTOR plays critical roles in regulating many physiological processes including erythropoiesis. It is composed of two distinct complexes, mTORC1 and mTORC2, which differ in their components and downstream signaling effects. Our previous study revealed that the inhibition of mTORC1 by rapamycin significantly repressed the erythroid progenitor expansion in the early stage but promoted enucleation and mitochondria clearance in the late stage of erythroid differentiation. However, the particular roles and differences of mTORC1 and mTORC2 in the regulation of erythropoiesis still remain largely unknown. In the present study, we investigated the comparative effects of dual mTORC1/mTORC2 mTOR kinase inhibitor AZD8055 and mTORC1 inhibitor rapamycin on erythroid differentiation in K562 cells induced by hemin and erythropoiesis in β-thalassemia mouse model. In vitro erythroid differentiation model of hemin-induced K562 cells and β-thalassemia mouse model were treated with AZD8055 and rapamycin. Cell Counting Kit-8 was used to detect cell viability. The cell proliferation, cell cycle, erythroid surface marker expression, mitochondrial content, and membrane potential were determined and analyzed by flow cytometry and laser scanning confocal microscopy. Globin gene expression during erythroid differentiation was measured by RT-qPCR. The mTORC2/mTORC1 and autophagy pathway was evaluated using western blotting. Both AZD8055 and rapamycin treatments increased the expression levels of the erythroid differentiation-specific markers, CD235a, -globin, -globin, and -globin. Notably, AZD8055 suppressed the cell proliferation and promoted the mitochondrial clearance of hemin-induced K562 cells more effectively than rapamycin. In a mouse model of -thalassemia, both rapamycin and AZD8055 remarkably improve erythroid cell maturation and anemia. Moreover, AZD8055 and rapamycin treatment inhibited the mTORC1 pathway and enhanced autophagy, whereas AZD8055 enhanced autophagy more effectively than rapamycin. Indeed, AZD8055 treatment inhibited both mTORC2 and mTORC1 pathway in hemin-induced K562 cells. AZD8055 is more effective than rapamycin in inhibiting proliferation and promoting mitochondrial clearance in erythroid differentiation, which might provide us one more therapeutic option other than rapamycin for ineffective erythropoiesis treatment in the future. These findings also provide some preliminary information indicating the roles of mTORC1 and mTORC2 in erythropoiesis, and further studies are necessary to dissect the underlying mechanisms.

This study aims to study how gold nanoparticles (AuNPs) function in the recruitment and polarization of tumor-associated macrophages (TAMs) in hormone-sensitive prostate cancer (HSPC) and castration-resistant prostate cancer (CRPC). Phorbol ester (PMA)-treated THP-1 cells were cocultured with LNCaP or PC3 cells to simulate TAMs. Macrophage M2 polarization levels were detected using flow cytometry and M2 marker determination. ATG5 expression was detected by western blotting. Luciferase reporter assay was used to analyze the N6-methyladenosine (mA) site activity of ATG5 3' untranslated regions (3'-UTRs). Methylated RNA immune precipitation (MeRIP)-quantitative polymerase chain reaction (qPCR) was performed to determine the mA levels at ATG5 3'-UTR. Xenograft mouse models were used to determine the function of AuNPs in vivo. Macrophages exhibited reduced M2 polarization in both HSPC and CRPC cells after AuNP treatment which was prevented by induction of autophagy. AuNP treatment decreased the mA levels in the 3'-UTR of ATG5. Mutational analysis of potential mA sites within ATG5 3'-UTR revealed that these sites were required for AuNP regulation, indicating that AuNPs inhibited ATG5 levels in an mA-dependent manner. The mouse model revealed that AuNPs significantly reduced the M2 polarization of TAMs in an autophagy-dependent manner in vivo. This suggests that AuNPs inhibit tumor growth in vivo partially through targeting M2 TAM. The ATG5/autophagy pathway is inhibited by AuNP treatment in an METTL3/mA-dependent manner. AuNPs inhibit the TAM M2 polarization in HSPC and CRPC by inhibiting ATG5/autophagy.

The present study aimed to analyze the impact of astragaloside IV (AS-IV) on abdominal aortic aneurysm (AAA) and the glycocalyx, elucidating the potential mechanism of AS-IV.

Trauma and burns are leading causes of death and significant global health concerns. RNA-binding proteins (RBPs) play a crucial role in post-transcriptional gene regulation, influencing various biological processes of cellular RNAs. This study aims to review the emerging trends and key areas of research on RBPs in the context of trauma and burns. A series of relevant articles were manually reviewed, and scientific publications on RBPs related to trauma and burns were retrieved from the Web of Science Core Collection (WoSCC) on May 19, 2024. Bibliometric analysis was performed using R-bibliometrix, VOSviewer, and CiteSpace. We adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to conduct the meta-analysis, followed by a comprehensive review of the selected papers. A total of 539 publications were identified from 2000 to 2024. China was the most productive and collaborative country, with Zhang Y being the most prolific author and PLoS One being the leading publication source. Keyword analysis revealed four distinct clusters. The thematic analysis identified eight key topics, including "RNA-binding proteins," "traumatic brain injury," and "inflammation." Four studies involving 5.976 patients were included in the final meta-analysis, which indicated a correlation between RBP expression levels and poor prognosis in traumatic brain injury (TBI). Our findings provide valuable insights into the developing trends and key areas of research on RBPs in trauma and burns. Notably, we identified two primary hotspots: RBPs in the pathophysiological mechanisms of various traumatic injuries and RBPs in the processes of cutaneous wound healing. This rapidly evolving field offers significant reference points for scientific researchers and clinical practitioners.

Shock wave therapy (SWT) is a new alternative therapy for patients with severe coronary artery disease that improves myocardial ischemic symptoms by delivering low-energy shock wave stimulation to ischaemic myocardium with low-energy pulsed waves. However, the specific mechanism of its protective effect is not fully understood, especially for the protective mechanism in cardiomyocytes after hypoxia/reoxygenation (H/R). We selected a rat H9c2 cardiomyocyte cell line to establish a stable H/R cardiomyocyte injury model by hypoxia/reoxygenation, and then used SWT for therapeutic intervention to explore its cardiomyocyte protective mechanisms. The results showed that SWT significantly increased cell viability and GSH levels while decreasing LDH levels, ROS levels, and MDA levels. SWT also improved mitochondrial morphology and function of cells after H/R. Meanwhile, we found that SWT could increase the expression of GPX4, xCT, and Bcl-2, while decreasing the expression of Bax and cleaved caspase-3, and inhibiting cardiomyocyte apoptosis and ferroptosis. Moreover, this protective effect of SWT on cardiomyocytes could be significantly reversed by knockdown of xCT, a key regulator protein of ferroptosis. In conclusion, our study shows that SWT can attenuate hypoxia-reoxygenation-induced myocardial injury and protect cardiomyocyte function by inhibiting H/R-induced apoptosis and ferroptosis, and this therapy may have important applications in the treatment of clinical myocardial ischemic diseases.

Benign prostate hyperplasia (BPH) is common in elderly men. Previously, paddy waste (both husk and straw) reportedly had chemopreventive potential. The main aim of this study was to explore the chemopreventive properties of paddy waste against prostate disease. This study determines the antiproliferative activity of the paddy waste product in spontaneously hypertensive rats (SHRs). Aqueous methanol extracts of paddy husk and straw were administered to SHRs for 17 weeks via drinking water, with no observed toxicity on dietary intake, body weight, liver, or kidney. The study used 18 male SHRs to model primary hypertension and 6 male Wistar Kyoto (WKY) rats as normotensive controls. The SHRs were divided into three groups: control ( = 6), paddy husk treated ( = 6, 15 mg/kg), and paddy straw treated ( = 6, 15 mg/kg), with treatment delivered in drinking water. It managed to reduce blood pressure (72.0 mmHg;   < 0.01) and the size of the ventral prostate to around 0.05% (  < 0.01). Histological analysis revealed antiproliferative signs such as a reduction in the number of acini (7.50;   < 0.01), epithelial height (10.55 µm;   < 0.01), and epithelial acinar area (18.17%;   < 0.01). Aqueous methanol extracts have arrested the cell cycle by downregulating (  < 0.01) proliferative marker, Ki-67, and proliferating cell nuclear antigen (PCNA). Prostate cell growth is arrested by downregulation of androgen receptor (AR) which inhibited AR mRNA transcription (RTPCR analysis) and induced cell cycle arrest at the S phase through p27 and cyclin E2 (western blot analysis). In conclusion, paddy waste product especially husk is a better chemopreventive agent against prostate disease.