Diabetic cardiomyopathy (DCM) is a multifaceted cardiovascular disorder in which immune dysregulation plays a pivotal role. The immunological molecular mechanisms underlying DCM are poorly understood.

In this editorial, we commented on two articles published online in August and September 2024 in the , which focused on modifying the gut microbiota (GM) to prevent or delay the progression of diabetes mellitus (DM) and DM-related complications. Numerous studies, many of which are animal studies, have indicated the potential role of GM in the pathogenesis of DM. However, the detailed causality and mechanisms between GM and DM have not been fully clarified. Although there have been some reports of a potential role of modifying the GM in treating DM, most lack long-term observations and are not mechanistic. Additionally, the GM and its role in DM might vary among individuals; therefore, GM-targeted interventions should be individualized to realize their therapeutic potential.

Since the discovery of insulin over 100 years ago, the focus of research in the management of type 1 diabetes (T1D) has centered around glycemic control and management of complications rather than the prevention of autoimmune destruction of pancreatic β cells. Fortunately, in recent years, there has been significant advancement in immune-targeted pharmacotherapy to halt the natural progression of T1D. The immune-targeted intervention aims to alter the underlying pathogenesis of T1D by targeting different aspects of the immune system. The immunotherapy can either antagonize the immune mediators like T cells, B cells or cytokines (antibody-based therapy), or reinduce self-tolerance to pancreatic β cells (antigen-based therapy) or stem-cell treatment. Recently, the US Food and Drug Administration approved the first immunotherapy teplizumab to be used only in stage 2 of T1D. However, the window of opportunity to practically implement this approved molecule in the selected target population is limited. In this Editorial, we briefly discuss the various promising recent developments in the field of immunotherapy research in T1D. However, further studies of these newer therapeutic agents are needed to explore their true potential for prevention or cure of T1D.

Diabetic nephropathy (DN) is a severe microvascular complication of diabetes characterized by inflammation, oxidative stress, and renal fibrosis. Asiaticoside (AC) exhibits anti-inflammatory, antioxidant, and anti-fibrotic properties, suggesting potential therapeutic benefits for DN. This study aimed to investigate the protective effects of AC against DN and elucidate the underlying mechanisms involving the nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) antioxidant pathway.

Current treatment strategies for diabetic retinopathy (DR), an eye condition that can lead to blindness, have mainly focused on proliferative DR, including vitreous injection, retinal photocoagulation, and vitrectomy. Vitreous injections mainly depend on anti-vascular endothelial growth factor therapy. In this editorial, we comment on the article by Sun . We focus specifically on the mechanisms of the protective effect of genipin on the retina. Genipin is a gardenia extract used in traditional Chinese medicine (TCM). In their study, the authors suggest that controlling advanced glycosylation by the intraocular injection of genipin may be a strategy for preventing retinopathy. The innovative use of a Chinese medicine extract injected into the eye to achieve a curative effect has attracted our attention. Although TCM is effective in treating DR, the topical application of DR, especially intraocular injections, is not yet feasible. Herein, we present a brief analysis of effective Chinese medicines for the treatment of DR. The effectiveness of local injections of TCM applied directly into the eyes holds promise as an effective treatment approach for DR.

Diabetes mellitus (DM) is one of the major causes of mortality worldwide, with inflammation being an important factor in its onset and development. This review summarizes the specific mechanisms of the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway in mediating inflammatory responses. Furthermore, it comprehensively presents related research progress and the subsequent involvement of this pathway in the pathogenesis of early-stage DM, diabetic gastroenteropathy, diabetic cardiomyopathy, non-alcoholic fatty liver disease, and other complications. Additionally, the role of cGAS-STING in autonomic dysfunction and intestinal dysregulation, which can lead to digestive complications, has been discussed. Altogether, this study provides a comprehensive analysis of the research advances regarding the cGAS-STING pathway-targeted therapeutic agents and the prospects for their application in the precision treatment of DM.

Diabetic foot (DF) is a serious complication of type 2 diabetes. This study aimed to investigate the factors associated with DF occurrence and the role of delayed medical care in a cohort of patients with type 2 diabetes.

In this editorial, we comment on the article by He , specifically in relation to the efficacy of bariatric surgery glucagon-like peptide-1 receptor agonist (GLP-1RA) therapy in the management of type 2 diabetes (T2D) associated with obesity. Bariatric surgery has now also been shown to be safe and effective in pre-teens and teenagers with obesity and T2D, but information on newer GLP-1RAs in these groups is predictably limited. In older individuals (age > 65 years), both bariatric surgery and GLP-1RA therapy improve cardiovascular outcomes. Bariatric surgery is not infrequently associated with post-operative postprandial hypoglycemia, which is not the case with GLP-1RAs and, paradoxically, there is evidence that GLP-1RAs may reduce both the frequency and severity of postprandial hypoglycemia. Comparative trials of the long-term efficacy of bariatric surgery and GLP-1RAs are indicated.

In patients with type 2 diabetes mellitus (T2DM), the risk of hypoglycemia also occurs in at a time-in-range (TIR) of > 70%. The hemoglobin glycation index (HGI) is considered the best single factor for predicting hypoglycemia, and offers new perspectives for the individualized treatment of patients with well-controlled blood glucose levels that are easily ignored in clinical settings.

In this editorial, we discuss an article by Wang , focusing on the role of mitochondria in peripheral insulin resistance and insulin secretion. Despite numerous and pre-clinical studies supporting the involvement of mitochondrial dysfunction and oxidative stress in the pathogenesis of diabetes and its complications, efforts to target mitochondria for glycemic control in diabetes using mitochondria-targeted antioxidants have produced inconsistent results. The intricate functionality of mitochondria is summarized to underscore the challenges it poses as a therapeutic target. While mitochondria-targeted antioxidants have demonstrated improvement in mitochondrial function and oxidative stress in pre-clinical diabetes models, the results regarding glycemic control have been mixed, and no studies have evaluated their hypoglycemic effects in diabetic patients. Nonetheless, pre-clinical trials have shown promising outcomes in ameliorating diabetes-related complications. Here, we review some reasons why mitochondria-targeted antioxidants may not function effectively in the context of mitochondrial dysfunction. We also highlight several alternative approaches under development that may enhance the targeting of mitochondria for diabetes treatment.

Dyslipidemia and type 2 diabetes mellitus (T2DM) are chronic conditions with substantial public health implications. Effective management of lipid metabolism in patients with T2DM is critical. However, there has been insufficient attention given to the relationship between thyroid hormone sensitivity and dyslipidemia in the T2DM population, particularly concerning non-high-density lipoprotein cholesterol (non-HDL-C).

Diabetic cardiomyopathy (DCM), a complication of diabetes, poses a significant threat to public health, both its diagnosis and treatment presents challenges. Teneligliptin has promising applications and research implications in the treatment of diabetes mellitus. Zhang observed the therapeutic effect of teneligliptin on cardiac function in mice with DCM. They validated that teneligliptin's mechanism of action in treating DCM involves cardiomyocyte protection and inhibition of inflammasome activity. Given that the inflammasome plays a crucial role in the onset and progression of DCM, it presents a promising therapeutic target. Nevertheless, further clinical validation is required to ascertain the preventive and therapeutic efficacy of teneligliptin in DCM.

Cardiopulmonary bypass (CPB) is a common procedure in cardiac surgery. CPB is a high-risk factor for acute kidney injury (AKI), and diabetes is also such a factor. Diabetes can lead to copper overload. It is currently unclear whether AKI after CPB in diabetic patients is related to copper overload.

Interleukin-35 (IL-35) is a novel protein comprising IL-12α and IL-27β chains. The IL12A and genes are responsible for its production. The study of IL-35 has experienced a substantial increase in interest in recent years, as demonstrated by many research papers. Recent clinical studies have shown that individuals who do not have a C-peptide have notably reduced amounts of IL-35 in their blood serum. This is accompanied by a drop in the percentage of IL-35 Treg cells, regulatory B cells, and CD8 FOXP3 cells that produce IL-35. This article em-phasizes the potential significance of IL-35 expression in governing the immune response and its involvement in chronic inflammatory autoimmune diabetes in pancreatic inflammation. It demonstrates IL-35's ability to regulate cytokine proportions, modulate B cells, and protect against autoimmune diabetes. However, further investigation is necessary to ascertain the precise mechanism of IL-35, and meticulous planning is essential for clinical studies.

In this editorial, we comment on the article by Zhang . Chronic kidney disease (CKD) presents a significant challenge in managing glycemic control, especially in diabetic patients with diabetic kidney disease undergoing dialysis or kidney transplantation. Conventional markers like glycated haemoglobin (HbA1c) may not accurately reflect glycemic fluctuations in these populations due to factors such as anaemia and kidney dysfunction. This comprehensive review discusses the limitations of HbA1c and explores alternative methods, such as continuous glucose monitoring (CGM) in CKD patients. CGM emerges as a promising technology offering real-time or retrospective glucose concentration measure-ments and overcoming the limitations of HbA1c. Key studies demonstrate the utility of CGM in different CKD settings, including hemodialysis and peritoneal dialysis patients, as well as kidney transplant recipients. Despite challenges like sensor accuracy fluctuation, CGM proves valuable in monitoring glycemic trends and mitigating the risk of hypo- and hyperglycemia, to which CKD patients are prone. The review also addresses the limitations of CGM in CKD patients, emphasizing the need for further research to optimize its utilization in clinical practice. Altogether, this review advocates for integrating CGM into managing glycemia in CKD patients, highlighting its superiority over traditional markers and urging clinicians to consider CGM a valuable tool in their armamentarium.

Glucagon-like peptide-1 receptor agonists (GLP-1RA) and sodium-glucose co-transporter-2 inhibitors (SGLT-2I) are associated with significant cardiovascular benefit in type 2 diabetes (T2D). However, GLP-1RA or SGLT-2I alone may not improve some cardiovascular outcomes in patients with prior cardiovascular co-morbidities.

It is widely recognized that chronic hyperglycemia decreases bone quality, although little is known about the impact of the rapid correction of chronic hyperglycemia on the quality of bone remodeling. This spotlight article explores this correlation by focusing on the stages of bone remodeling linked to glucose levels.

This editorial introduces the potential of targeting macrophage function for diabetic cardiomyopathy (DCM) treatment by dipeptidyl peptidase-4 (DPP-4) inhibitors. Zhang studied teneligliptin, a DPP-4 inhibitor used for diabetes management, and its potential cardioprotective effects in a diabetic mouse model. They suggested teneligliptin administration may reverse established markers of DCM, including cardiac hypertrophy and compromised function. It also inhibited the NLRP3 inflammasome and reduced inflammatory cytokine production in diabetic mice. Macrophages play crucial roles in DCM pathogenesis. Chronic hyperglycemia disturbs the balance between pro-inflammatory (M1) and anti-inflammatory (M2) macrophages, favoring a pro-inflammatory state contributing to heart damage. Here, we highlight the potential of DPP-4 inhibitors to modulate macrophage function and promote an anti-inflammatory environment. These compounds may achieve this by elevating glucagon-like peptide-1 levels and potentially inhibiting the NLRP3 inflammasome. Further studies on teneligliptin in combination with other therapies targeting different aspects of DCM could be suggested for developing more effective treatment strategies to improve cardiovascular health in diabetic patients.

The increasing prevalence of diabetes has led to a growing population of end-stage kidney disease (ESKD) patients with diabetes. Currently, kidney transplantation is the best treatment option for ESKD patients; however, it is limited by the lack of donors. Therefore, dialysis has become the standard treatment for ESKD patients. However, the optimal dialysis method for diabetic ESKD patients remains controversial. ESKD patients with diabetes often present with complex conditions and numerous complications. Furthermore, these patients face a high risk of infection and technical failure, are more susceptible to malnutrition, have difficulty establishing vascular access, and experience more frequent blood sugar fluctuations than the general population. Therefore, this article reviews nine critical aspects: Survival rate, glucose metabolism disorder, infectious complications, cardiovascular events, residual renal function, quality of life, economic benefits, malnutrition, and volume load. This study aims to assist clinicians in selecting individualized treatment methods by comparing the advantages and disadvantages of hemodialysis and peritoneal dialysis, thereby improving patients' quality of life and survival rates.

Diabetes is often associated with gastrointestinal dysfunctions, which can lead to hypoglycemia. Dexmedetomidine (DEX) is a commonly used sedative in perioperative diabetic patients and may affect gastrointestinal function.

Type II diabetes mellitus (T2DM) has experienced a dramatic increase globally across countries of various income levels over the past three decades. The persistent prevalence of T2DM is attributed to a complex interplay of genetic and environmental factors. While numerous pharmaceutical therapies have been developed, there remains an urgent need for innovative treatment approaches that offer effectiveness without significant adverse effects. In this context, the exploration of the gut microbiome presents a promising avenue. Research has increasingly shown that the gut microbiome of individuals with T2DM exhibits distinct differences compared to healthy individuals, suggesting its potential role in the disease's pathogenesis and progression. This emerging field offers diverse applications, particularly in modifying the gut environment through the administration of prebiotics, probiotics, and fecal microbiome transfer. These inter-ventions aim to restore a healthy microbiome balance, which could potentially alleviate or even reverse the metabolic dysfunctions associated with T2DM. Although current results from clinical trials have not yet shown dramatic effects on diabetes management, the groundwork has been laid for deeper investigation. Ongoing and future clinical trials are critical to advancing our understanding of the microbiome's impact on diabetes. By further elucidating the mechanisms through which microbiome alterations influence insulin resistance and glucose metabolism, researchers can develop more targeted interventions. The potential to harness the gut microbiome in developing new therapeutic strategies offers a compelling prospect to transform the treatment landscape of T2DM, potentially reducing the disease's burden significantly with approaches that are less reliant on traditional pharmaceuticals and more focused on holistic, systemic health improvements.