MOTS-c regulates the ROS/TXNIP/NLRP3 pathway to alleviate diabetic cardiomyopathy.

Chronic low-grade inflammation is a characteristic of diabetes, which often culminates in cardiovascular events including myocardial damage, thereby increasing the risk of debilitating cardiac complications. The mitochondria-derived peptide MOTS-c regulates glucose and lipid metabolism while improving insulin resistance, making it a potential candidate for the treatment of diabetes and cardiovascular diseases. We investigated the impact of MOTS-c on cardiac structure and inflammation in diabetic rats induced by a high-sugar-fat diet combined with low-dose streptozotocin (30 mg/kg, i.

The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.

Myocardial remodeling and dysfunction are commonly observed in type 2 diabetes mellitus (T2DM). Aerobic exercise can partly alleviate diabetes-induced myocardial dysfunction through its antioxidant actions. MOTS-c is a potential exercise mimic.

MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats.

Cardiac structure remodeling and dysfunction are common complications of diabetes, often leading to serious cardiovascular events. MOTS-c, a mitochondria-derived peptide, regulates metabolic homeostasis by accelerating glucose uptake and improving insulin sensitivity. Plasma levels of MOTS-c are decreased in patients with diabetes.

MOTS-c and aerobic exercise induce cardiac physiological adaptation via NRG1/ErbB4/CEBPβ modification in rats.

Aims: To determine the effects of the mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c) and aerobic exercise on cardiac structure and function and explore the role of neuregulin-1 (NRG1)- ErbB2 receptor tyrosine kinase 4(ErbB4)- CCAAT-enhancer binding protein β (C/EBPβ) in cardiac physiological adaptation induced by MOTS-c and aerobic training.

Main Methods: We used Hematoxylin-Eosin staining(HE)and Transmission Electron Microscope (TEM) to observe the cardiac myocardial structure, carotid artery catheterization to test cardiac function, and real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting to describe the changes of NRG1, ErbB4, C/EBPβ, and Gata in cardiac physiological adaptation.

Key Findings: MOTS-c and aerobic training significantly increased heart weight and heart weight index (HWI) (all p < 0.

Time-dependent Effects of Moderate- and High-intensity Exercises on Myocardial Transcriptomics.

The heart is a highly adaptable organ that responds to changes in functional requirements due to exposure to internal and external stimuli. Physical exercise has unique stimulatory effects on the myocardium in both healthy individuals and those with health disorders, where the effects are primarily determined by the intensity and recovery time of exercise. We investigated the time-dependent effects of different exercise intensities on myocardial transcriptional expression in rats.

MOTS-c and Exercise Restore Cardiac Function by Activating of NRG1-ErbB Signaling in Diabetic Rats.

Pathologic cardiac remodeling and dysfunction are the most common complications of type 2 diabetes. Physical exercise is important in inhibiting myocardial pathologic remodeling and restoring cardiac function in diabetes. The mitochondrial-derived peptide MOTS-c has exercise-like effects by improving insulin resistance, combatting hyperglycemia, and reducing lipid accumulation.

The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats.

Cardiac remodeling is a physiological adaptation to aerobic exercise and which is characterized by increases in ventricular volume and the number of cardiomyocytes. The mitochondrial derived peptide MOTS-c functions as an important regulator in physical capacity and performance. Exercise elevates levels of endogenous MOTS-c in circulation and in myocardium, while MOTS-c can significantly enhance exercise capacity.

Exercise modulates heat shock protein 27 activity in diabetic cardiomyopathy.

Aims: Heat shock protein 27 regulates homeostasis of skeletal and cardiac muscle proteins in various stressful states including diabetes and exercise. Aerobic exercise can inhibit or ameliorate cardiac structural abnormality and dysfunction in diabetic cardiomyopathy. The aim of this study was to evaluate the role of HSP27 in aerobic exercise improving cardiac diastolic dysfunction in type 2 diabetic rats.