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Copyright: ©Author(s) 2026.
World J Diabetes. Jul 15, 2026; 17(7): 119712
Published online Jul 15, 2026. doi: 10.4239/wjd.119712
Figure 1
Figure 1 Shared pathophysiological links underpinning diabetes-centered five-condition co-management and cardiovascular risk. A: Insulin resistance serves as a central hub linking hyperglycemia/diabetes, hypertension, dyslipidemia, and obesity, thereby promoting vascular endothelial dysfunction, activation of the renin-angiotensin system, and atherogenesis; B: A chronic low-grade inflammatory network, reflected by elevated cytokines and inflammatory biomarkers (e.g., tumor necrosis factor-α, interleukin-1, interleukin-6, and C-reactive protein), contributes to endothelial injury and plaque initiation and progression; C: Oxidative stress and endothelial dysfunction arise from increased reactive oxygen species generation and reduced antioxidant capacity, resulting in decreased nitric oxide bioavailability, impaired vasomotor regulation, and a procoagulant milieu; D: Metabolite accumulation-associated toxicity (including urate- and lipid/glucose-related signals) can activate the NOD-like receptor family pyrin domain containing 3 inflammasome, amplifying systemic inflammation and reinforcing the interconnected progression of cardiometabolic abnormalities. CRP: C-reactive protein; IL: Interleukin; NLRP3: NOD-like receptor family pyrin domain containing 3; TNF-α: Tumor necrosis factor-α.


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