ArticleScientific reports2026
NOP2-mediated m5C methylation impairs mitophagy and aggravates acute lung injury by targeting PINK1.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sepsis-induced acute lung injury (ALI) involves complex pathological mechanisms. 5-methylcytosine (m5C) RNA modification, catalyzed by methyltransferases like NOP2, plays a crucial role in regulating inflammation and cellular processes. However, the role of NOP2 and its potential regulation of m5C modification in sepsis-induced ALI remains unclear. An in vitro ALI model was established by treating human pulmonary epithelial A549 cells with lipopolysaccharide (LPS). Inflammatory cytokine levels (IL-1β, IL-6, TNF-α) were measured by ELISA. Apoptosis was assessed by flow cytometry. Mitophagy was evaluated via immunofluorescence staining for mitochondrial Parkin and western blot analysis of Parkin, LC3-II, COX IV, and p62. The m5C modification of PINK1 mRNA was analyzed by m5C-RIP-PCR. The specific m5C site was identified using bioinformatics and validated by dual-luciferase reporter assays. LPS treatment significantly upregulated NOP2 expression in A549 cells. Knockdown of NOP2 attenuated LPS-induced inflammation, apoptosis, and promoted mitophagy, as evidenced by increased Parkin translocation, elevated LC3-II levels, and decreased p62 and COX IV levels. Mechanistically, NOP2 knockdown reduced m5C modification on PINK1 mRNA, particularly at site 197, thereby enhancing PINK1 mRNA stability and increasing its expression. Furthermore, knockdown of PINK1 reversed the protective effects of NOP2 knockdown on inflammation, apoptosis, and mitophagy in LPS-treated A549 cells. NOP2 is upregulated in LPS-induced ALI models. Its knockdown alleviates cellular injury by reducing the m5C modification of PINK1 mRNA, which enhances PINK1 expression and promotes mitophagy. The NOP2/m5C/PINK1 axis represents a novel regulatory pathway in sepsis-induced ALI, suggesting potential therapeutic targets for its treatment.
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