miR-21: a central regulator of fibrosis not only in the broken heart: EXPERT'S PERSPECTIVE

This editorial refers to an article by S. Roy et al . [5][1] published in Cardiovascular Research in 2009. It is accompanied by a retrospective editorial by two of the authors of that original article, C.K. Sen and S. Roy, pp. 230–233, this issue, as part of this Spotlight on Landmark Papers in Cardiovascular Research . Adverse remodelling of the heart associated with hypertension, valve disease, or myocardial infarction includes diverse functional, structural, and metabolic abnormalities, such as sarcomere disorganization, cardiomyocyte loss, and interstitial and perivascular fibrosis, ultimately leading to left ventricular hypertrophy, dilatation, and failure.1,2MicroRNAs, endogenous single-stranded molecules consisting of ∼22 non-coding nucleotides, are important regulators of cardiovascular (patho)physiology.2–4 The work by the group of C.K. Sen appearing in Cardiovascular Research early in 20095 was among the first (i) to recognize the importance of microRNAs for ischaemic injury of the heart, (ii) to characterize the expression of a specific microRNA, miR-21, in a time-dependent and cell-specific manner, and (iii) to define a specific target gene and pathophysiological response.Reactive myocardial fibrosis is associated with reduced microvascular network and disruption of normal myocardial structures, and results from an excessive deposition of extracellular matrix by fibroblasts. While reactive fibrosis accompanying hypertrophy in response to pressure overload … [1]: #ref-5