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. 2025 Jan 27.
doi: 10.1007/s10528-025-11040-3. Online ahead of print.

Angiotensin-Converting Enzyme 2 Enhances Autophagy via the Consumption of miR-326 in a Mouse Model of Acute Lung Injury

Xingsheng Lin  1 , Fengying Gao  2
Affiliations

Angiotensin-Converting Enzyme 2 Enhances Autophagy via the Consumption of miR-326 in a Mouse Model of Acute Lung Injury

Xingsheng Lin et al. Biochem Genet. .

Abstract

Angiotensin-converting enzyme 2 (ACE2) has been reported to exert a protective effect in acute lung injury (ALI), though its underlying mechanism remains incompletely understood. In this study, ACE2 expression was found to be upregulated in a mouse model of ALI induced by lipopolysaccharide (LPS) injection. ACE2 knockdown modulated the severity of ALI, the extent of autophagy, and the mTOR pathway in this model. ACE2 regulated liver kinase B1 (LKB1) gene expression by sequestering miR-326, thereby alleviating ALI severity through enhanced autophagy. In cell-based experiments, miR-326 was shown to regulate ACE2 and LKB1 expression and autophagy. Overexpression of ACE2 disrupted miR-326's regulatory effect on LKB1, suggesting that LKB1 may function as an endogenous sponge for miR-326. These findings imply that elevated ACE2 expression in lung could play enhance the autophagy via the consumption of miR-326.

Keywords: Acute lung injury; Angiotensin-converting enzyme 2; Autophagy; Lung vascular endothelial cells; MiRNA.

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Conflict of interest statement

Declarations. Conflict of interest: There is no competing interest. Ethical Approval: Approval for all experimental protocols was granted by the Animal Care Committee of Shengli Clinical Medical College of Fujian Medical University.

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