Proteomics and microRNA profiling in cardiac fibrosis

Cardiac fibrosis is characterized by the deposition of extracellular matrix (ECM) and mediated by cardiac fibroblasts via the renin-angiotensin system (RAS) and transforming growth factor beta (TGFβ) signaling pathways. Recognition of TGFβ by fibroblasts leads to myofibroblast differentiation as well as induction of ECM protein expression. An imbalance between proand anti-fibrotic signals results in excessive ECM deposition, which is linked to arrhythmogenicity, and defective systolic and diastolic function. Since ECM proteins accumulate over time, the balance of protein synthesis and degradation is particularly important in the context of cardiac fibrosis. Additionally, microRNAs (miRNAs) target messenger RNAs (mRNAs) and control their degradation or translation into proteins, affecting both the dynamics and the composition of cardiac ECM. Proteomics and miRNA profiling are novel research tools for discovering biomarkers and therapeutic targets in disease. Bioinformatic integration of proteomics and miRNA profiling experiments will further our understanding of the balance between repair and pathological processes in cardiac fibrosis.