Pulmonary Hypertension and Obesity: Focus on Adiponectin

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Pulmonary hypertension is an umbrella term including many different disorders causing an increase of the mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg. Recent data revealed a strong association between obesity and pulmonary hypertension. Adiponectin is a protein synthetized by the adipose tissue with pleiotropic effects on inflammation and cell proliferation, with a potential protective role on the pulmonary vasculature. Both in vivo and in vitro studies documented that adiponectin is an endogenous modulator of NO production and interferes with AMP-activated protein kinase (AMPK) activation, mammalian target of rapamycin (mTOR), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ) signaling preventing endothelial dysfunction and proliferation. Furthermore, adiponectin ameliorates insulin resistance by mediating the biological effects of peroxisome proliferator-activated receptor-gamma (PPARγ). Therefore, adiponectin modulation emerged as a theoretical target for the treatment of pulmonary hypertension, currently under investigation. Recently, consistent data showed that hypoglycemic agents targeting PPARγ as well as renin⁻angiotensin system inhibitors and mineralocorticoid receptor blockers may influence pulmonary hemodynamics in different models of pulmonary hypertension.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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