Cardiomyocyte apoptosis and ventricular remodeling pathways

Cardiomyocyte apoptosis and ventricular remodeling pathways encompass the complex series of molecular and cellular changes that occur in the heart following a myocardial infarction (MI). These processes involve the programmed death of heart muscle cells and the subsequent structural reorganization of the ventricular wall, which can lead to heart failure (StatPearls, PMID: 30725820). Key molecular drivers include the activation of the renin-angiotensin-aldosterone system (RAAS), increased oxidative stress, and the release of pro-inflammatory cytokines like TNF-alpha and TGF-beta (PubMed, PMID: 28471767). While these pathways are not a single molecular target, they are the primary focus of post-MI therapeutic strategies aimed at preserving cardiac function. Drugs such as ACE inhibitors, beta-blockers, and mineralocorticoid receptor antagonists are used to modulate these pathways by reducing hemodynamic load and inhibiting maladaptive signaling (NIH, NHLBI). Understanding these pathways is crucial for developing novel therapies that can specifically target apoptotic regulators or promote myocardial regeneration. Monitoring biomarkers like NT-proBNP and troponins helps clinicians assess the extent of remodeling and the efficacy of treatment.

Other names

Post-MI remodelingCardiac remodelingMyocardial apoptosis signalingLeft ventricular remodeling

Pharmacological agents target these pathways by inhibiting the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, thereby reducing wall stress, inflammation, and pro-apoptotic signaling in the myocardium.