Emphysema and chronic bronchitis characterize chronic obstructive pulmonary disease (COPD), which makes it difficult for patients to breathe. Wempe, De-Zolt and colleagues partly alleviated the pathological effects associated with COPD in the lungs of an emphysema mouse model by genetically inactivating sestrin 2 (sesn2). Sesn2 induces the expression of signaling molecules that promote elastin breakdown. Sesn2 inhibition may protect lung elastin from degradation, thereby promoting lung elasticity and function in COPD patients.

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