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Life sciences · Journal article
Cells · October 13, 2026
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Obesity-induced adipose tissue remodeling results from the interplay of metabolic stress, chronic inflammation, extracellular matrix remodeling, and vascular dysfunction. Beyond their established role in thrombosis, platelets have emerged as immunometabolic effectors at the interface between vascular and metabolic responses. This review examines mechanistic, translational, and clinical evidence supporting a platelet–adipose tissue axis and its relevance to obesity-associated cardiometabolic disease. In obesity and related metabolic disorders, platelets display a hyperreactive phenotype characterized by alterations in glycolysis, mitochondrial function, oxidative stress, and secretory activity, together with changes in extracellular vesicle biogenesis and cargo. Through direct cellular interactions and soluble or vesicle-mediated signaling, platelets may influence leukocyte recruitment, macrophage phenotype, fibroblast activation, extracellular matrix remodeling, and endothelial or adipocyte metabolic pathways relevant to adipose tissue dysfunction. However, the extent of direct platelet-dependent effects within adipose tissue is poorly known. We propose that these mechanisms may participate in a feed-forward thromboinflammatory circuit in which metabolic stress promotes platelet reprogramming, while platelet-derived signals may in turn amplify endothelial dysfunction, inflammation, fibrosis, and impaired adipose tissue plasticity. Although direct causal evidence in humans remains limited, current data support a biologically coherent framework in which platelets may act as amplifiers of adipose tissue dysfunction rather than established primary drivers. Overall, this platelet–adipose tissue axis may provide a framework for investigating novel molecular pathways relevant to cardiometabolic risk stratification and therapeutic strategies.