Ventricular remodeling

**Ventricular remodeling** refers to the structural and functional changes in the size, shape, architecture, and performance of the ventricles—most commonly the left ventricle—following cardiac injury or chronic stress. This process can be adaptive or maladaptive. Pathological ventricular remodeling is typically triggered by myocardial infarction but may also result from chronic hypertension, valvular disease, cardiomyopathy, or volume overload. The process involves myocyte hypertrophy/apoptosis and interstitial fibrosis leading to chamber dilation and altered geometry; these changes are associated with progressive decline in systolic function and increased risk for morbidity/mortality in heart failure patients[1][3][7]. Therapeutic strategies aim to prevent or reverse maladaptive remodeling using drugs that target neurohormonal pathways such as ACE inhibitors/ARBs/beta-blockers/aldosterone antagonists; device therapies like cardiac resynchronization may also be used. Biomarkers for monitoring include imaging modalities like echocardiography/MRI as well as circulating markers reflecting systemic inflammation/fibrosis. **Note:** "Ventricular remodeling" is a pathophysiological process—not a discrete molecular entity such as a receptor/enzyme/transporter—and thus is not considered a direct therapeutic target itself. Instead, it represents an outcome/process influenced by multiple molecular targets within various signaling pathways involved in cardiovascular adaptation/injury response[2][6]. Therefore: is_target should be **false** is_incorrect should be **true**, because this entry does not correspond to a single molecule/receptor but rather describes a complex biological phenomenon involving many targets. If you need information on specific molecular targets involved in ventricular remodeling—such as angiotensin II type 1 receptor (AT1R), mineralocorticoid receptor (MR), transforming growth factor-beta (TGFβ), etc.—please specify which one you are interested in.

Other names

Cardiac remodelingLeft ventricular remodelingPost-infarction ventricular remodeling

Inhibition of neurohormonal activation (renin–angiotensin system, sympathetic nervous system)[9] - Reduction of cardiac afterload and preload[8]