Role of fibroblasts in the pathophysiology of heart failure with preserved ejection fraction. A literature review.

Abstract

The purpose of the article is to describe the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to examine the role of cardiac fibroblasts in this condition. HFpEF is characterized by a decreased pumping function of the heart, but with an ejection fraction within normal limits. In this pathology, left ventricular diastolic dysfunction occurs and several mechanisms have been proposed to explain this condition, including concentric hypertrophy and myocardial stiffness due to fibrosis and collagen accumulation, according to the scientific literature on the subject. Cardiac fibroblasts play a crucial role in the development and perpetuation of myocardial fibrosis in HFpEF. These cells are activated in response to injury and produce collagen and other extracellular matrix proteins to repair damaged tissue. However, in HFpEF, there is excessive and prolonged activation of fibroblasts, leading to excessive production of connective tissue and the formation of rigid scars that make it difficult for the left ventricle to relax. Abnormal fibroblast phenotypes in HFpEF, similar to cancer-associated fibroblasts, have been proposed to contribute to fibrosis and disease progression, resulting in cardiac hypertrophy and impaired calcium management, within the characteristic manifestations of the pathology in question.