Stress signals (such as hemodynamic overload) activate signal transduction pathways that lead to either the upregulation or downregulation of specific miRNAs. Stress signals that increase the expression levels of miRNAs can result in the downregulation of several target mRNAs through gene silencing or, more commonly, translational blockade of the target mRNA. Alternatively, a stress-induced decrease in the expression levels of inhibitory miRNAs can lead to upregulation of previously suppressed target genes. Ultimately, it is the miRNA-induced pattern of change in gene expression that contributes to the resultant disease phenotype.
Reproduced with permission from [71].