Novel anti-fibrotic therapies, including epigenetic modifications and CRISPR technologies, show promise in addressing cardiac fibrosis following myocardial infarction.
This review outlines emerging preclinical strategies, such as epigenetic modifications and CRISPR technologies, for targeting cardiac fibrosis after myocardial infarction.
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Cardiac fibrosis is a common pathological consequence of most myocardial diseases. It is associated with the excessive accumulation of extracellular matrix proteins as well as fibroblast differentiation into myofibroblasts in the cardiac interstitium. This structural remodeling often results in myocardial dysfunctions such as arrhythmias and impaired systolic function in patients with heart conditions, ultimately leading to heart failure and death. An understanding of the precise mechanisms of cardiac fibrosis is still limited due to the numerous signaling pathways, cells, and mediators involved in the process. This review article will focus on the pathophysiological processes associated with the development of cardiac fibrosis. In addition, it will summarize the novel strategies for anti-fibrotic therapies such as epigenetic modifications, miRNAs, and CRISPR technologies as well as various medications in cellular and animal models.
Raziyeva et al. (Fri,) reported a other. Novel anti-fibrotic therapies, including epigenetic modifications and CRISPR technologies, show promise in addressing cardiac fibrosis following myocardial infarction.