Targeting Myocardial Fibrosis—A Magic Pill in Cardiovascular Medicine?

Abstract

Fibrosis, characterized by an excessive accumulation of extracellular matrix, has long been seen as an adaptive process that contributes to tissue healing and regeneration. More recently, however, cardiac fibrosis has been shown to be a central element in many cardiovascular diseases (CVDs), contributing to the alteration of cardiac electrical and mechanical functions in a wide range of clinical settings. This paper aims to provide a comprehensive review of cardiac fibrosis, with a focus on the main pathophysiological pathways involved in its onset and progression, its role in various cardiovascular conditions, and on the potential of currently available and emerging therapeutic strategies to counteract the development and/or progression of fibrosis in CVDs. We also emphasize a number of questions that remain to be answered, and we identify hotspots for future research.

Microneedle Patch Loaded with Exosomes Containing MicroRNA‐29b Prevents Cardiac Fibrosis after Myocardial Infarction

“…Currently, the approaches for preventing cardiac fibrosis after MI generally involve i) application of biomaterials (e.g., injectable hydrogels and cardiac patches), to support the infarcted tissue and reduce elevated wall stress, [10][11][12][13][14][15][16] and ii) delivery of antifibrotic drugs or bioactive factors to inhibit specific signaling pathways related to fibrosis (e.g., transforming growth factor-𝛽 (TGF-𝛽)-related signaling pathways that play a dominant role in myocardial fibrosis by inducing the transformation of cardiac fibroblasts into myofibroblasts and promoting the production and deposition of collagens). [17][18][19][20][21] Recently, microRNAs (miRNAs), a class of small noncoding RNAs that play crucial roles in regulating gene expression, have been discovered to treat fibrosis. [22] In particular, the miRNA-29 (miR-29) family shows antifibrotic activity and therapeutic value in the setting of disorders associated with tissue fibrosis by regulating the TGF-𝛽 signaling pathway and targeting genes that encode ECM proteins associated with fibrosis.…”

Autonomic imbalance and atrial ectopic activity—a pathophysiological and clinical view

“…A wide array of cardiac and non-cardiac conditions act as major risk factors for atrial arrhythmias, particularly AF, by promoting atrial proarrhythmic electrical and structural remodeling (Şerban and Scridon, 2018;Scridon and Balan, 2022). Numerous systemic (e.g., obesity, diabetes mellitus, hypertension, obstructive sleep apnea, aging, sustained endurance training) and cardiac (e.g., heart failure, cardiomyopathies, acute and chronic ischemic heart disease) conditions have also been shown to induce structural and/or functional autonomic alterations, further promoting atrial arrhythmogenicity (Figure 6).…”

3D Spheroids — a Cellular Model for Studying the Effects of Hypoxia on the Epicardial Microenvironment

“…На протяжении нескольких десятков лет сердечно-сосудистые заболевания занимают лидирующие позиции среди причин заболеваемости и смертности населения в России и во всем мире [1]. Важнейшим фактором прогрессирования большинства этих заболеваний является фиброз, связанный с избыточным отложением белков внеклеточного матрикса, в частности -фибриллярного коллагена, что ведет к повышению жесткости миокарда, потере систолической функции и развитию выраженных структурно-морфологических изменений [2,3]. В последние годы появились свидетельства того, что активацию процессов фиброза может вызывать множество различных факторов, которые реализуют разноплановое воздействие на клетки, что определяет особенности и скорость течения патологического процесса [4].…”