Pulmonary cold sensing through Club cells triggers adipose thermogenesis to ameliorate obesity.
Pulmonary cold sensing via Club cells activates adipose thermogenesis, with KCNK2 channels mediating cold detection in the lungs of mice.
- Why it matters: Understanding how peripheral organs contribute to thermoregulation could reveal new targets for obesity treatment, addressing gaps in knowledge about lung-based cold sensing.
- What they did: Using CC10-Cre and AAV-based mouse models, the study identified KCNK2 channels in bronchial Club cells as cold sensors that increase Irisin secretion through Ca²⁺ fluctuations, promoting thermogenesis.
- The result: Pharmacological activation of this pathway with fluoxetine boosts thermogenesis and reduces obesity in mice, suggesting a novel lung-based approach for anti-obesity therapies.