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Platelet Disorders and Treatments · Journal article
Undergraduate Research in Natural and Clinical Science and Technology (urncst) Journal · August 10, 2026
Raises a question worth testing. It does not answer one.
This narrative review proposes that platelet dysfunction acts as a key mediator linking obesity and dysglycemia to cardiovascular disease through multiple signalling pathways involving endothelial damage, oxidative stress, and immune cell crosstalk. It is a hypothesis-generating synthesis rather than an evidence summary, clarifying proposed molecular mechanisms without reporting original or aggregated clinical trial data.
Journal article.
Cardiovascular complications accounted for more than 19.8 million deaths in 2022, approximately 32% of all global fatalities Platelet dysfunction is proposed as a key mediator that transduces and amplifies damage across multiple organ systems in cardiometabolic disease Obesity-induced oxidative stress overproduces reactive oxygen species that oxidize lipoproteins and platelet phospholipids, creating a prothrombotic endothelial surface
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This is a mechanistic review article proposing platelet dysfunction as a key mediator in cardiometabolic disease pathogenesis, without reporting primary experimental or clinical evidence.
Quoted from the source exactly as published.
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Cardiometabolic diseases are a framework focusing on two metabolic drivers, adiposity and dysglycemia, which give rise to type 2 diabetes mellitus and cardiovascular diseases, including coronary artery disease, heart failure, and atrial fibrillation. Among all, cardiovascular complications are most lethal, accounting for more than 19.8 million deaths in 2022 — approximately 32% of all global fatalities. The pathogenesis is a multi-organ crosstalk between heightened platelet activity and persistent low-grade inflammation. Platelet dysfunction acts as a key mediator that transduces and amplifies damage across multiple systems. Platelets are activated by factors released from damaged endothelium, extending spiky pseudopods and secreting granules that promote adhesion and aggregation. Obesity is a principal causative factor in the development of metabolic syndromes, characterized by hyperlipidemia and hypercholesterolemia, which overproduce reactive oxygen species, thereby oxidizing lipoproteins and platelet phospholipids. These radicals and free fatty acids transform the endothelium into a prothrombotic and pro-inflammatory surface vulnerable to ischemic clot formation. Type 2 diabetes mellitus is a Dysglycemia-Based Chronic Disease. Insulin resistance, a major contributor to the disruption of plasma glucose metabolism, is induced by platelet-degranulating factors that trigger autoimmune attack on insulin receptors and enhanced oxidative stress. Cardiovascular disease is driven by the mutual interaction between platelets and immune cells (leukocytes). Cholesterol accumulation causes platelets to release pro-inflammatory chemokines and recruit macrophages engulfing cholesterol, forming the lipid core of atherosclerotic plaques. The plaques are prone to the oxidative stress of the hypertensive circulatory system, thereby being scraped off, blocking blood flow, and leading to heart failure and stroke. Atrial fibrillation is marked by a thromboembolic state in the cardiac and valvular structures, where cardiac cells are exposed to platelet activators, inflammatory molecules, and coagulating molecules. First-line therapy for cardiometabolic diseases aims to reduce thrombus formation by targeting the ligands, receptors, and activators for platelet activation. However, addressing the upstream metabolic syndromes is considered the ultimate solution to prevent cardiometabolic diseases. This review clarifies the molecular signalling pathways by which platelets contribute to the progression of cardiometabolic diseases, as well as their concerning risk factors and treatments for platelet hyperactivity and hyperaggregability.
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