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Multiple extracellular matrix (ECM) components and immune cells in cardiac tissue constitute the cardiac microenvironment, a dynamic system essential for maintaining heart structure and function. The ECM, composed of proteins like collagen, elastin, and fibronectin, provides mechanical support and acts as a reservoir for signaling molecules, while immune cells, including resident macrophages and infiltrating lymphocytes, monitor tissue integrity and respond to injury (Frangogiannis, 2019, Circulation Research). In cardiovascular diseases such as myocardial infarction and heart failure, this system undergoes significant dysregulation, characterized by excessive collagen deposition (fibrosis) and chronic inflammation (Swirski & Nahrendorf, 2018, Nature Reviews Immunology). Therapeutic interventions targeting this environment seek to modulate immune cell phenotypes and inhibit pathological ECM remodeling to preserve cardiac output and prevent ventricular dilation. Understanding the complex crosstalk between these components is critical for developing regenerative therapies and improving long-term outcomes in patients with cardiac remodeling (Borg & Caulfield, 2002, Nature Reviews Molecular Cell Biology).
Modulation of the cardiac microenvironment through inhibition of the renin-angiotensin-aldosterone system (RAAS), reduction of pro-fibrotic signaling, and regulation of inflammatory cell infiltration to prevent maladaptive remodeling.
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