SQSTM1 is a therapeutic target for infection and sterile inflammation

Tang, Daolin; Kang, Rui

doi:10.1016/j.cyto.2023.156317

Cited by 4 publications

(1 citation statement)

References 121 publications

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“…S100a9 and Itih4 have the role of regulating inflammatory response ( Wang et al, 2018 ; Ma et al, 2021 ). Chil3 ( Yoshimura and Oppenheim, 2011 ) and Sqstm1 ( Tang and Kang, 2023 ) were reported to be activated or released in large quantities during inflammatory states. Collectively, AAI exposure placed the kidneys in an inflammatory state.…”

Section: Discussionmentioning

confidence: 99%

Delineation of renal protein profiles in aristolochic acid I-induced nephrotoxicity in mice by label-free quantitative proteomics

Liu,

Wu,

Peng

et al. 2024

Front. Pharmacol.

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Introduction: Aristolochic acid nephropathy (AAN) is a kidney injury syndrome caused by aristolochic acids exposure. Our study used label-free quantitative proteomics to delineate renal protein profiles and identify key proteins after exposure to different doses of aristolochic acid I (AAI).Methods: Male C57BL/6 mice received AAI (1.25 mg/kg/d, 2.5 mg/kg/d, or 5 mg/kg/d) or vehicle for 5 days.Results and discussion: The results showed that AAI induced dose-dependent nephrotoxicity. Differences in renal protein profiles between the control and AAI groups increased with AAI dose. Comparing the control with the low-, medium-, and high-dose AAI groups, we found 58, 210, and 271 differentially expressed proteins, respectively. Furthermore, protein-protein interaction network analysis identified acyl-CoA synthetase medium-chain family member 3 (Acsm3), cytochrome P450 family 2 subfamily E member 1 (Cyp2e1), microsomal glutathione S-transferase 1 (Mgst1), and fetuin B (Fetub) as the key proteins. Proteomics revealed that AAI decreased Acsm3 and Cyp2e1 while increasing Mgst1 and Fetub expression in mice kidneys, which was further confirmed by Western blotting. Collectively, in AAI-induced nephrotoxicity, renal protein profiles were dysregulated and exacerbated with increasing AAI dose. Acsm3, Cyp2e1, Mgst1, and Fetub may be the potential therapeutic targets for AAN.

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