Diabetes mellitus (DM) is a complex global pandemic that frequently leads to multiple complications. Diabetic cardiomyopathy (DCM) is the primary cause of heart failure in patients with type 1 and 2 diabetes and is fundamentally characterized by abnormalities in myocardial structure and function. Metabolic disorders occupy a leading role in the pathogenesis of DCM, manifesting as disrupted substrate metabolism, dysregulated signaling pathways, and energy imbalance. Given the limited benefits of conventional therapeutic strategies targeting glucolipid metabolism, increasing research efforts have focused on amino acid metabolism. Amino acids are involved in the synthesis of nitrogen-containing compounds and serve as an energy source under specific conditions. Moreover, emerging studies demonstrate that metabolic disturbances of specific amino acids—such as branched-chain amino acids (BCAAs), glutamine, and arginine—exacerbate mitochondrial dysfunction and oxidative stress, thereby promoting myocardial fibrosis and cardiomyocyte injury. Therefore, this review aims to summarize the general characteristics and regulatory pathways of amino acid metabolism, as well as the specific mechanisms by which metabolic alterations of amino acids contribute to the pathogenesis and progression of diabetic cardiomyopathy, with the hope of advancing more effective translational therapeutic approaches.

Background: Diabetes significantly increases the risk of atrial fibrillation (AF), but identifying high-risk individuals remains a clinical challenge. This study aimed to improve AF risk stratification in diabetic patients through a combination of clinical modeling and untargeted metabolomic analysis. Methods: A clinical risk score was developed using data from the National Health and Nutrition Examination Survey (NHANES) and validated in an independent cohort from Tongji Hospital. Its association with long-term outcomes and its ability to predict AF recurrence after catheter ablation were assessed in follow-up studies. Additionally, untargeted plasma metabolomics was performed in a subset of diabetic patients with and without AF to explore underlying mechanism. Results: The risk score showed good predictive performance in both the development and validation cohorts and was significantly associated with clinical prognosis. When combined with left atrial diameter and AF type, it also improved the prediction of AF recurrence after ablation. Metabolomic profiling revealed notable disturbances in energy metabolism, heightened inflammatory activity, and elevated stress responses in AF patients, indicating a distinct metabolic risk profile. Conclusions: This study provided two approaches to identify high-risk AF in diabetic patients, discussed the underlying pathophysiological mechanisms, and compared their characteristics and applications. And integrated strategies could improve AF risk stratification and personalized management in the diabetic.

Cardiovascular diseases (CVDs) remain the leading cause of disability and mortality worldwide, characterized by highly complex pathophysiological mechanisms involving multilayered gene regulatory networks. Despite substantial advances in related research in recent years, the annual number of CVD-related deaths continues to rise, imposing a profound and persistent global socioeconomic burden. Consequently, there is an urgent need to identify novel molecular mechanisms and therapeutic targets. As an emerging class of non-coding RNAs, tRNA-derived small RNAs (tsRNAs) have increasingly been recognized as pivotal regulators of cardiovascular homeostasis. By targeting RNA, proteins, or other molecular structures, tsRNAs are deeply involved throughout the initiation, progression, and clinical outcomes of CVDs by orchestrating key pathological processes, including mitochondrial dysfunction, metabolic reprogramming, and inflammatory responses. Meanwhile, with ongoing advances in high-throughput sequencing technologies and therapeutic development strategies, the clinical translation of tsRNAs as novel biomarkers and therapeutic targets is also accelerating. Therefore, this review aims to systematically summarize the current core consensus and the latest research advances in this field, comprehensively elucidate the specific mechanisms by which tsRNAs contribute to the pathogenesis and progression of CVDs, and provide innovative insights for the development of more effective translational strategies.