Key result
Transcriptional regulators, microRNAs, and histone deacetylases emerge as promising targets for novel anti-fibrotic therapies.
This review highlights emerging molecular targets for the development of specific anti-fibrotic therapies in ischemic and non-ischemic heart disease.
Premature for clinical use in cardiac fibrosis; leaves open targeted trials of these molecular pathways.
Cardiac fibrosis, characterized by excessive accumulation of extracellular matrix, abolishes cardiac contractility, impairs cardiac function, and ultimately leads to heart failure. In recent years, significant evidence has emerged that supports the highly dynamic and responsive nature of the cardiac extracellular matrix. Although our knowledge of cardiac fibrosis has advanced tremendously over the past decade, there is still a lack of specific therapies owing to an incomplete understanding of the disease etiology and process. In this review, we attempt to highlight some of the recently investigated molecular determinants of ischemic and non-ischemic fibrotic remodeling of the myocardium that present as promising avenues for development of anti-fibrotic therapies.
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Wang et al. (2018) conducted a review in Cardiac fibrosis. Molecular therapeutic targets (Transcription factors, miRNAs, HDACs) was evaluated. Molecular therapeutic targets, including transcriptional regulators, microRNAs, and histone deacetylases, present promising avenues for the development of novel anti-fibrotic therapies.
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