Abstract
The heart can respond to increased pathophysiological demand through alterations in tissue structure and function . This process, called cardiac remodeling, is particularly evident following myocardial infarction (MI), where the blockage of a coronary artery leads to widespread death of cardiac muscle. Following MI, necrotic tissue is replaced with extracellular matrix (ECM), and the remaining viable cardiomyocytes (CMs) undergo hypertrophic growth. ECM deposition and cardiac hypertrophy are thought to represent an adaptive response to increase structural integrity and prevent cardiac rupture. However, sustained ECM deposition leads to the formation of a fibrotic scar that impedes cardiac compliance and can induce lethal arrhythmias. Resident cardiac fibroblasts (CFs) are considered the primary source of ECM molecules such as collagens and fibronectin, particularly after becoming activated by pathologic signals. CFs contribute to multiple phases of post-MI heart repair and remodeling, including the initial response to CM death, immune cell (IC) recruitment, and fibrotic scar formation. The goal of this review is to describe how resident fibroblasts contribute to the healing and remodeling that occurs after MI, with an emphasis on how fibroblasts communicate with other cell types in the healing infarct scar (–).