Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Abstract

Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI). The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways and various types of cells in time-dependent manners. Our understanding of the development of cardiac fibrosis after MI has evolved in basic and clinical researches, and the regulation of fibrotic remodeling may facilitate novel diagnostic and therapeutic strategies, and finally improve outcomes. Here, we aim to elaborate pathophysiology, examination and intervention of cardiac fibrosis after MI.

Keywords: antifibrotic therapy; cardiac remodeling; extracellular matrix; fibroblast; fibrosis; myocardial infarction; myofibroblast.

FIGURE 1

The molecular mechanisms of cardiac fibrosis. Note: Akt, protein kinase B; EGF, epidermal growth factor; ERK, extracellular signal-regulated kinase; FGF, fibroblast growth factor; HO-1, heme oxygenase-1; IL-1, interleukin-1; IL-4, interleukin-4; JAK, janus kinase; JNK, c-Jun N-terminal kinase; NF-κB, nuclear factor kappa-B; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; STAT, signal transducer and activator of transcription 3; TGF-β, transforming growth factor β.

FIGURE 2

Summary of the interventions of cardiac fibrosis. Note: CAR, chimeric antigen receptor; NLRP3: nod-like receptor protein three; RAAS: renin-angiotensin-aldosterone system; SGLT2-i: sodium-glucose cotransporter-2 inhibitor; TGF-β: transforming growth factor β.