Why the study?
The precise contribution of adipokines to myocardial remodelling and heart failure, particularly in obesity, remains to be determined due to the complex balance between pro- and anti-remodelling factors.
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Dual adipokine effects in obese remodeling merit mechanistic studies; leaves open clinical translation.
It is now widely recognized that adipocytes have the ability to produce a myriad of bioactive compounds released into the circulation and affecting distal organs, including the heart. These factors, termed adipokines, are also produced by various tissues in addition to adipocytes, including cardiac tissue, and have the ability to modulate cardiac function and the response to pathology. Among the processes greatly affected by adipokines is myocardial remodelling due to hypertrophy and fibrosis, two processes that contribute to the development of heart failure. This is particularly relevant under conditions of obesity, and the accompanying increased adiposity, in general, results in increased adipokine production. The effects of adipokines on cardiac remodelling can be both beneficial or adverse, depending on the adipokine type, such as adiponectin and leptin, respectively. The molecular bases underlying the effects of adipokines on myocardial remodelling have been extensively studied and likely involve a multiplicity of cell signalling processes, thus demonstrating substantial complexity. Emerging evidence suggests that these proteins play an important role in cardiac pathology. Their precise contribution is yet to be determined with certainty, as this likely reflects a balance between pro-remodelling and anti-remodelling factors.
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Karmazyn et al. (2025) studied this question.
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