Key result
TRPV1 activation protects against diabetic cardiomyopathy by reducing oxidative stress, inflammation, and mitochondrial dysfunction.
Why the study?
Activating TRPV1 channels can improve diabetes-related complications including cardiomyopathy, but the specific mechanisms and cardioprotective effects remain unclear.
Does TRPV1 channel activation prevent or improve diabetic cardiomyopathy in diabetic models?
Does TRPV1 channel activation prevent or improve diabetic cardiomyopathy in diabetic models?
Activating TRPV1 presents a potential novel therapeutic target for preventing and treating diabetes-induced cardiovascular complications such as diabetic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
TRPV1 activation may mitigate diabetic cardiomyopathy in models; leaves open clinical translation pending prospective human trials.
Cardiovascular disease, especially heart failure (HF) is the leading cause of death in patients with diabetes. Individuals with diabetes are prone to a special type of cardiomyopathy called diabetic cardiomyopathy (DCM), which cannot be explained by heart diseases such as hypertension or coronary artery disease, and can contribute to HF. Unfortunately, the current treatment strategy for diabetes-related cardiovascular complications is mainly to control blood glucose levels; nonetheless, the improvement of cardiac structure and function is not ideal. The transient receptor potential cation channel subfamily V member 1 (TRPV1), a nonselective cation channel, has been shown to be universally expressed in the cardiovascular system. Increasing evidence has shown that the activation of TRPV1 channel has a potential protective influence on the cardiovascular system. Numerous studies show that activating TRPV1 channels can improve the occurrence and progression of diabetes-related complications, including cardiomyopathy; however, the specific mechanisms and effects are unclear. In this review, we summarize that TRPV1 channel activation plays a protective role in the heart of diabetic models from oxidation/nitrification stress, mitochondrial function, endothelial function, inflammation, and cardiac energy metabolism to inhibit the occurrence and progression of DCM. Therefore, TRPV1 may become a latent target for the prevention and treatment of diabetes-induced cardiovascular complications.
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Bao et al. (2023) conducted a review in Diabetic cardiomyopathy and diabetes-induced cardiovascular complications. TRPV1 channel activation was evaluated. TRPV1 channel activation exerts cardioprotective effects in diabetic models by attenuating oxidative stress, mitochondrial dysfunction, endothelial dysfunction, and inflammation to inhibit diabetic cardiomyopathy.
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