The Platelet–Adipose Tissue Axis in Metabolic Disease: From Platelet Reprogramming to Tissue Remodeling
- 1Unit of Neuro-Cardiovascular Axis, Centro Cardiologico Monzino IRCCS, 20138 Milan, Italy
- 2Department of Biology and Biotechnology “L. Spallanzani”, Università degli Studi di Pavia, Via Bassi 21, 27100 Pavia, Italy
- 3Department of Theoretical and Applied Sciences, eCampus University, 22060 Novedrate, Italy
Abstract
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.
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BibTeX
@article{simone2026plateletadipose,
title = {{The Platelet–Adipose Tissue Axis in Metabolic Disease: From Platelet Reprogramming to Tissue Remodeling}},
author = {Rosa Simone and Cosimo Damiano Perrone and Valentina Lemmo and Chiara Lonobile and Silvia Stella Barbieri},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15201863},
url = {https://www.mdpi.com/2073-4409/15/20/1863},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Platelet–Adipose Tissue Axis in Metabolic Disease: From Platelet Reprogramming to Tissue Remodeling
AU - Rosa Simone
AU - Cosimo Damiano Perrone
AU - Valentina Lemmo
AU - Chiara Lonobile
AU - Silvia Stella Barbieri
PY - 2026
DA - 2026/10/13
JO - Cells
DO - 10.3390/cells15201863
UR - https://www.mdpi.com/2073-4409/15/20/1863
AB - 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.
SN - 2073-4409
ER -