Chair and Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, 02-091 Warsaw, Poland.
Int J Mol Sci. 2022 Apr 11;23(8):4195. doi: 10.3390/ijms23084195.
Obesity is a growing epidemiological problem, as two-thirds of the adult population are carrying excess weight. It is a risk factor for the development of cardiovascular diseases (hypertension, ischemic heart disease, myocardial infarct, and atrial fibrillation). It has also been shown that chronic obesity in people may be a cause for the development of heart failure with preserved ejection fraction (HFpEF), whose components include cellular hypertrophy, left ventricular diastolic dysfunction, and increased extracellular collagen deposition. Several animal models with induced obesity, via the administration of a high-fat diet, also developed increased heart fibrosis as a result of extracellular collagen accumulation. Excessive collagen deposition in the extracellular matrix (ECM) in the course of obesity may increase the stiffness of the myocardium and thereby deteriorate the heart diastolic function and facilitate the occurrence of HFpEF. In this review, we include a rationale for that process, including a discussion about possible putative factors (such as increased renin-angiotensin-aldosterone activity, sympathetic overdrive, hemodynamic alterations, hypoadiponectinemia, hyperleptinemia, and concomitant heart diseases). To address the topic clearly, we include a description of the fundamentals of ECM turnover, as well as a summary of studies assessing collagen deposition in obese individuals.
肥胖是一个日益严重的流行病学问题，因为三分之二的成年人口超重。它是心血管疾病（高血压、缺血性心脏病、心肌梗死和心房颤动）发展的一个危险因素。此外，人们已经发现，慢性肥胖可能是射血分数保留性心力衰竭（HFpEF）发展的一个原因，其组成部分包括细胞肥大、左心室舒张功能障碍和细胞外胶原沉积增加。通过给予高脂肪饮食诱导肥胖的几种动物模型，由于细胞外胶原积累，也会导致心脏纤维化增加。在肥胖过程中细胞外基质（ECM）中胶原的过度沉积可能会增加心肌的硬度，从而恶化心脏舒张功能，并促进 HFpEF 的发生。在这篇综述中，我们提出了这一过程的基本原理，包括讨论可能的潜在因素（如肾素-血管紧张素-醛固酮活性增加、交感神经兴奋过度、血液动力学改变、脂联素减少、瘦素增加和并存的心脏病）。为了清楚地阐述这一主题，我们还描述了 ECM 周转的基本原理，并总结了评估肥胖个体胶原沉积的研究。
