LncRNA as a regulator in the development of diabetic complications.

Diabetes is a metabolic disease characterized by hyperglycemia, which induces the production of AGEs, ROS, inflammatory cytokines, and growth factors, leading to the formation of vascular dysfunction and target organ damage, promoting the development of diabetic complications. Diabetic nephropathy, retinopathy, and cardiomyopathy are common complications of diabetes, which are major contributors to disability and death in people with diabetes. Long non-coding RNAs affect gene transcription, mRNA stability, and translation efficiency to influence gene expression for a variety of biological functions. Over the past decade, it has been demonstrated that dysregulated long non-coding RNAs are extensively engaged in the pathogenesis of many diseases, including diabetic complications. Thus, this review discusses the regulations of long non-coding RNAs on the primary pathogenesis of diabetic complications (oxidative stress, inflammation, fibrosis, and microvascular dysfunction), and some of these long non-coding RNAs may function as potential biomarkers or therapeutic targets for diabetic complications.

Impact of the gut microbiota on angiotensin â ¡-related disorders and its mechanisms.

The renin-angiotensin system (RAS) consists of multiple angiotensin peptides and performs various biological functions mediated by distinct receptors. Angiotensin II (Ang II) is the major effector of the RAS and affects the occurrence and development of inflammation, diabetes mellitus and its complications, hypertension, and end-organ damage via the Ang II type 1 receptor. Recently, considerable interest has been given to the association and interaction between the gut microbiota and host. Increasing evidence suggests that the gut microbiota may contribute to cardiovascular diseases, obesity, type 2 diabetes mellitus, chronic inflammatory diseases, and chronic kidney disease. Recent data have confirmed that Ang II can induce an imbalance in the intestinal flora and further aggravate disease progression. Furthermore, angiotensin converting enzyme 2 is another player in RAS, alleviates the deleterious effects of Ang II, modulates gut microbial dysbiosis, local and systemic immune responses associated with coronavirus disease 19. Due to the complicated etiology of pathologies, the precise mechanisms that link disease processes with specific characteristics of the gut microbiota remain obscure. This review aims to highlight the complex interactions between the gut microbiota and its metabolites in Ang II-related disease progression, and summarize the possible mechanisms. Deciphering these mechanisms will provide a theoretical basis for novel therapeutic strategies for disease prevention and treatment. Finally, we discuss therapies targeting the gut microbiota to treat Ang II-related disorders.