Myocardial Interstitial Fibrosis in Heart Failure

Abstract

Myocardial interstitial fibrosis contributes to left ventricular dysfunction leading to the development of heart failure. Basic research has provided abundant evidence for the cellular and molecular mechanisms behind this lesion and the pathways by which it imparts a detrimental impact on cardiac function. Translation of this knowledge, however, to improved diagnostics and therapeutics for patients with heart failure has not been as robust. This is partly related to the paucity of biomarkers to accurately identify myocardial interstitial fibrosis and to the lack of personalized antifibrotic strategies to treat it in an effective manner. This paper summarizes current knowledge of the mechanisms and detrimental consequences of myocardial interstitial fibrosis, discusses the potential of circulating and imaging biomarkers available to recognize different phenotypes of this lesion and track their clinical evolution, and reviews the currently available and potential future therapies that allow its individualized management in heart failure patients.

Does Chronic Kidney Disease Facilitate Malignant Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction of Hypertensive Origin?

“…Diffuse myocardial fibrosis (MF) is practically a constant finding in hypertensive patients with heart failure (HF) and contributes to left ventricular (LV) stiffness and dysfunction [1]. In hypertensive patients with HF, MF is the result of increased deposition of collagen type I fibers with increased cross-linking [1].…”

“…Diffuse myocardial fibrosis (MF) is practically a constant finding in hypertensive patients with heart failure (HF) and contributes to left ventricular (LV) stiffness and dysfunction [1]. In hypertensive patients with HF, MF is the result of increased deposition of collagen type I fibers with increased cross-linking [1]. In HF patients the amount of collagen deposition is associated with all-cause death [2], whereas in HF hypertensive patients the degree of collagen cross-linking is associated with the risk of hospitalization for HF [3].…”

Comprehensive Analysis and Co-Expression Network of mRNAs and lncRNAs in Pressure Overload-Induced Heart Failure

“…Heart failure (HF) is the end stage of various cardiovascular diseases, with high morbidity and mortality, leading to a significant burden on people's health (Ponikowski et al, 2016). Diverse pathophysiologic processes are involved in the failing heart, such as cardiomyocyte hypertrophy, myocardial fibrosis, energetic metabolism, ion channel disorder, and other pathways (Munzel et al, 2015;Zile et al, 2015;Gonzalez et al, 2018;Noordali et al, 2018). Cardiac pressure overload is one of the main mechanisms of HF, which can result in cardiac hypertrophy, cardiac structural remodeling, and electrical remodeling, related to over-expression or low-expression of functional genes and gene clusters (Nomura et al, 2018).…”

Myocardial interstitial matrix as novel target for succinic acid treatment strategies during experimental hypobaric hypoxia

“…Many of them are associated with sclerotic, fibrotic, autoimmune and inflammatory processes in which the extracellular myocardial matrix plays the crucial role by determining the adaptive and regenerative capabilities of myocardium [1]. The myocardial extracellular matrix is not just a passive entity, but rather a complex and dynamic microenvironment which represents an important structural and signaling system within the myocardium [2,3]. The network of collagen type I and III is associated with elastic fibers and binds the components of the myocardium together, retains the shape of the heart muscle and determines the mechanical properties of the myocardium during the cardiac cycle [4].…”

“…One of the most widespread forms of oxygen deficiency is hypoxic or hypobaric hypoxia [8]. Industrial development of mountain regions, military, sports, recreational and other activities, development of the Arctic and mineral resources of Russian Federation pose challenges to applied biology and medicine related to the development of methods of selection, optimization of adaptation processes and preservation of high human performance in extreme environmental conditions, which is impossible without understanding the mechanisms of adaptation of the heart to intermittent hypobaric hypoxia [3]. In the cells exposed to hypoxia reactive oxygen species (ROS) damage membranes (including mitochondrial), exacerbate the disturbances of energy metabolism, i.e.…”