Chronic cardiac stress induces pathologic hypertrophy and fibrosis of the myocardium. The
microRNA-29 (miR-29) family has been found to prevent excess collagen expression in …

Rationale: The adult heart is composed primarily of terminally differentiated, mature
cardiomyocytes that express signature genes related to contraction. In response to …

Background: Cardiac macrophages (cMPs) are increasingly recognized as important
regulators of myocardial homeostasis and disease, yet the role of noncoding RNA in these …

Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as a
key factor in the development of heart failure, but the mechanisms undelying cardiac fibrosis …

Regulation of gene expression during cardiac development and remodeling is very
complicated, involving epigenetic, transcriptional, post-transcriptional, and translational …

Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the
development of heart failure. Although dysregulation of microRNA (miRNA) is involved in …

Aims The overloaded heart remodels by cardiomyocyte hypertrophy and interstitial fibrosis,
which contributes to the development of heart failure. Signalling via the TGFβ-pathway is …

miR-21 is a 22-nucleotide long microRNA that matches target mRNAs in a complementary
base pairing fashion and regulates gene expression by repressing or degrading target …

Background miR-21 is a central regulator of cardiac fibrosis, and its inhibition in small-
animal models has been shown to be an effective antifibrotic strategy in various organs …

Increasing evidence suggests that microRNAs are intimately involved in the
pathophysiology of heart failure. MicroRNA-22 (miR-22) is a muscle-enriched miRNA …