Key result
Adipokines exert opposing effects on vascular homeostasis and inflammation in metabolic syndrome.
Why the study?
Dysregulated adipokine secretion may contribute to the link between metabolic syndrome and cardiocerebrovascular disease, but therapeutic potential and clinical validation remain unclear.
Adipokines serve as crucial mediators linking metabolic syndrome to cardiocerebrovascular events, and targeting these pathways (e.g., adiponectin/FGF21 signaling or IL-1/IL-6 inhibition) holds promising therapeutic potential.
Should not yet change clinical practice in metabolic syndrome; leaves open randomized trials of adipokine-targeted therapies.
Metabolic syndrome (MS), characterized by central obesity, hyperglycemia, hypertension, and dyslipidemia, substantially increases the risk of cardiovascular and cerebrovascular events. Adipose tissue is an active endocrine organ, and dysregulated adipokine secretion may contribute to the link between MS and vascular injury. In this narrative review, we synthesize evidence on adipokines implicated in MS-related cardiocerebrovascular disease and discuss their therapeutic potential. Adiponectin, fibroblast growth factor 21 (FGF21), and omentin are generally associated with improved insulin sensitivity, lipid handling, and endothelial homeostasis, whereas leptin, resistin, tumor necrosis factor-α, and interleukin-6 can promote inflammation and endothelial dysfunction through pathways including NF-κB and JAK/STAT. However, these associations may be modified by obesity, insulin resistance, disease stage, and other confounding factors, and some adipokines, such as adipsin, show context-dependent effects. Current translational evidence is strongest for strategies targeting adiponectin/FGF21 signaling and IL-1/IL-6-related inflammatory pathways, while evidence for cerebrovascular outcomes remains limited. Adipokine-directed interventions therefore remain promising but require rigorous clinical validation and disease-specific stratification.
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Wu et al. (2026) conducted a review in Metabolic syndrome and cardiocerebrovascular disease. Adipokines (adiponectin, FGF21, omentin, leptin, resistin, TNF-α, IL-6) was evaluated. Adiponectin, FGF21, and omentin improve homeostasis, whereas leptin, resistin, TNF-α, and IL-6 promote inflammation and endothelial dysfunction in metabolic syndrome.
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