EN | RU
EN | RU

Help Support

Back

Irisin: An essential player in combating diabetes, heart disease, and atherosclerosis

Diabetes Diabetes
Diabetes Diabetes

What's new?

Irisin transpires as a potential multifaceted therapeutic agent, combating gluconeogenesis, endothelial dysfunction, cardiomyocyte loss, and atherosclerosis in diabetic vascular ailments.

Irisin, primarily recognized as an exercise-induced chemokine, holds the potential to revolutionize therapeutic approaches used for diabetes and related cardiovascular ailments, as communicated by a novel review in the Biomedicine & Pharmacotherapy journal.

In the context of diabetes mellitus (DM), characterized by sedentary lifestyles and escalating lifespans, the role of exercise emerges as a potent antidote. Extensive research underscores the remarkable potential of exercise in modulating systemic metabolism, countering the dysregulation inherent in DM. Irisin, as a prominent exerkine, offers an exciting glimpse into this therapeutic landscape, initiating processes such as the browning of white adipose tissue through PGC-1α signalling, thereby enhancing energy expenditure. Irisin exhibits a multifaceted nature, exerting its influence on glucose metabolism through a myriad of mechanisms. It is effective in fighting against glucose dysmetabolism by curbing gluconeogenesis to promote glycogenesis. It has an eminent role in safeguarding endothelial function by stimulating nitric oxide production and reducing oxidative stress, thereby mitigating inflammation.

Concerning diabetic cardiomyopathy, it protects against cardiomyocyte loss and attenuates myocardial hypertrophy and fibrosis, making it a promising option in the realm of metabolic and cardiovascular therapeutics.

Source:

Biomedicine & Pharmacotherapy

Article:

New insights into the roles of Irisin in diabetic cardiomyopathy and vascular diseases

Authors:

Tiandong Zhang et al.

Comments (0)

You want to delete this comment? Please mention comment Invalid Text Content Text Content cannot me more than 1000 Something Went Wrong Cancel Confirm Confirm Delete Hide Replies View Replies View Replies en ru ua
Try: