The fat-heart entanglement and the role of 'osteopontin mechanics' in cardiometabolic senescence
Abstract
Background: Residual cardiovascular (CV) risk persists despite therapeutic advances. Obesity is heterogeneous, and visceral adipose tissue (VAT) dysfunction ('adiposopathy') complicates risk stratification. Osteopontin (OPN) is a pleiotropic mediator implicated in VAT inflammation, senescence-associated pathways, atherosclerosis and myocardial remodelling.
Methods: We performed a narrative synthesis of preclinical and clinical evidence on OPN across three domains: (i) VAT biology and senescence-associated secretory phenotype (SASP); (ii) atherosclerosis and plaque vulnerability; and (iii) myocardial fibrosis/remodelling and cardiometabolic heart failure. We also summarize biomarker and therapeutic implications.
Results: OPN is increased in obesity, particularly within VAT, where it contributes to SASP-related signalling, macrophage dysfunction, low-grade systemic inflammation, insulin resistance and cardiometabolic risk. Clinical and translational studies link circulating and tissue OPN levels to vascular inflammation, plaque vulnerability and adverse CV events. In the myocardium, OPN appears to act as a remodelling-specific mediator connecting extracardiac adiposity-related signals to interstitial fibrosis, with the strongest evidence in heart failure with preserved ejection fraction and diabetic cardiomyopathy. Across settings, OPN shows promise as an early biomarker for detection and risk stratification. Experimental modulation of OPN attenuates fibrosis and improves…
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