HIV-associated cardiomyopathy is driven by chronic immune-metabolic stress causing organelle dysfunction, which promotes myocardial stiffening despite viral suppression.
Proposes that HIV-associated myocardial remodeling is driven by unresolved organelle stress, highlighting opportunities for earlier intervention and prevention.
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People with HIV experience a disproportionate burden of myocardial fibrosis and diastolic dysfunction that is not fully explained by traditional cardiovascular risk factors or systemic inflammation. Emerging evidence suggests that HIV-associated cardiomyopathy originates from persistent disturbances in cardiomyocyte homeostasis driven by chronic immune-metabolic stress. Metabolic dysregulation, antiretroviral-related toxicity, and residual inflammatory signaling converge at the cardiomyocyte organelle level, leading to mitochondrial dysfunction, endoplasmic reticulum stress, and impaired autophagy. These interrelated processes precede overt structural heart disease and promote progressive myocardial stiffening, despite effective viral suppression. Framing myocardial remodeling as a consequence of unresolved organelle stress highlights opportunities for earlier intervention, including aggressive management of metabolic risk factors, the use of established cardioprotective therapies with antifibrotic effects, and emerging strategies targeting mitochondrial and proteostatic pathways. This organelle-centered perspective supports prevention-focused approaches that combine accessible imaging modalities and circulating biomarkers to mitigate the long-term cardiovascular risk in people with HIV, particularly in resource-limited settings.
Mutengo et al. (Thu,) reported a other. HIV-associated cardiomyopathy is driven by chronic immune-metabolic stress causing organelle dysfunction, which promotes myocardial stiffening despite viral suppression.