THE ROLE AND MECHANISM OF LONP1 IN THE SENESCENCE OF RENAL TUBULAR EPITHELIAL CELLS

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THE ROLE AND MECHANISM OF LONP1 IN THE SENESCENCE OF RENAL TUBULAR EPITHELIAL CELLS

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Co-author 1

Yuting Chen chenyuting_2019@163.com The First Affiliated Hospital of Nanjing Medical University Division of Nephrology, Department of Geriatrics Nanjing China -

Co-author 2

Nan Zhao 2022110216@stu.njmu.edu.cn The First Affiliated Hospital of Nanjing Medical University Division of Nephrology, Department of Geriatrics Nanjing China -

Co-author 3

Weihong Zhao zhaoweihongny@njmu.edu.cn The First Affiliated Hospital of Nanjing Medical University Division of Nephrology, Department of Geriatrics Nanjing China *

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Introduction

To investigate the role of mitochondrial Lon protease 1 (LONP1) in the senescence of renal tubular epithelial cells and its underlying molecular mechanisms.

Methods

This study employed both naturally aged mice and in vitro models of human renal tubular epithelial cells (HK-2) induced by D-galactose (D-gal), hydrogen peroxide (H₂O₂), and doxorubicin (DOX). Mitochondrial functional changes were assessed by evaluating the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), mitochondrial transcription factor A (TFAM), translocase of the outer mitochondrial membrane 20 (TOMM20), and dynamin-related protein 1 (DRP1). The expression levels and localization of LONP1 in aging kidney tissues and senescent HK-2 cells were detected using Western blotting and immunofluorescence (IF) staining. LONP1-overexpressing and knockdown HK-2 stable cell lines were established to analyze mitochondrial function-related proteins and cellular senescence markers using Western blotting. The extent of cellular senescence was assessed by real-time quantitative PCR (qRT-PCR) and senescence-associated beta-galactosidase (SA-β-gal) staining. Mechanistically, the impact of LONP1 knockdown on mitochondrial DNA (mtDNA) content, activation of the cGAS-STING signaling pathway, and expression of inflammatory cytokines IL-6 and IL-8 was further investigated using qRT-PCR and Western blot analysis.

Results

Mitochondrial dysfunction and reduced LONP1 expression were observed in both aged renal tissues and senescent HK-2 cells. Knockout of LONP1 exacerbated mitochondrial dysfunction and accelerated cellular senescence, while LONP1 overexpression improved mitochondrial function and delayed senescence. Mechanistically, LONP1 deficiency promoted the release of mtDNA, which activated the cGAS-STING pathway and triggered senescence-associated inflammation.

Conclusion

This study demonstrates that LONP1 plays a crucial role in regulating renal tubular epithelial cell senescence by maintaining mitochondrial homeostasis and inhibiting cGAS-STING-mediated inflammation. Our findings provide new insights into the mechanisms of kidney aging and suggest that LONP1 may be a potential therapeutic target for interventions aimed at renal aging and related pathologies.

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