Review Synthesizes Mechanisms, Therapeutic Targets for Obesity-Associated Cardiac Fibrosis

Cardiac fibrosis, a common pathological endpoint in various cardiac diseases, is a central determinant of heart failure progression. Obesity is a major global health challenge closely linked to cardiovascular disease, yet the specific mechanisms by which obesity drives cardiac fibrosis remain complex and incompletely understood. Current standard-of-care often addresses symptoms rather than the underlying pathological remodeling. This review aims to systematically synthesize these mechanisms and identify emerging therapeutic targets to bridge this knowledge gap.

This systematic review synthesized existing literature on the mechanisms underlying obesity-related cardiac fibrosis. Researchers elaborated on how various factors, including inflammatory factors, cytokines, and miRNAs, interact with adipose tissue and cardiac cells. The review then detailed the biological processes driven by these interactions, such as oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), autophagy dysregulation, and metabolic dysfunction. Finally, it examined potential therapeutic targets for preventing or reversing this condition.

The review identified a multifaceted pathological cascade leading to obesity-associated cardiac fibrosis. It highlighted that inflammatory factors, cytokines, and miRNAs play crucial roles by acting on both adipose tissue and cardiac cells. These interactions drive a series of detrimental biological processes within the heart. > The review found that obesity-associated cardiac fibrosis is primarily driven by oxidative stress, activation of the renin-angiotensin-aldosterone system, autophagy dysregulation, and profound metabolic dysfunction. These mechanisms collectively culminate in ventricular remodeling, heart failure, and atrial fibrillation. The synthesis also outlined several potential therapeutic targets aimed at interrupting these specific pathways to mitigate or reverse cardiac damage.