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Comprehensive Landscape of Post-Translational Modification Alterations in Nephrolithiasis Revealing Activation of Multiple Cell Death Pathways.

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Τίτλος: Comprehensive Landscape of Post-Translational Modification Alterations in Nephrolithiasis Revealing Activation of Multiple Cell Death Pathways.
Συγγραφείς: Dong Y; Department of Pharmacy, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China., Zhang M; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan250012, Shandong, China.; School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao266109, Shandong, China., Xu Y; Department of Urology, The Second Qilu Hospital of Shandong University, Jinan250033, Shandong, China., Zhang J; Department of Urology, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China., Wang C; Center for Translational Medicine Research, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China., Zhang X; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan250012, Shandong, China., Ni Y; Department of Urology, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China.
Πηγή: Journal of proteome research [J Proteome Res] 2026 Sep 04; Vol. 25 (9), pp. 4688-4703.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: American Chemical Society Country of Publication: United States NLM ID: 101128775 Publication Model: Print Cited Medium: Internet ISSN: 1535-3907 (Electronic) Linking ISSN: 15353893 NLM ISO Abbreviation: J Proteome Res Subsets: MEDLINE
Imprint Name(s): Original Publication: Washington, D.C. : American Chemical Society, c2002-
Ιατρικοί όροι (MeSH): Nephrolithiasis*/metabolism , Nephrolithiasis*/pathology , Nephrolithiasis*/genetics , Nephrolithiasis*/chemically induced , Protein Processing, Post-Translational*, Proteomics/methods ; Cell Death/genetics ; Kidney/metabolism ; Kidney/pathology ; Animals ; Mice ; Signal Transduction ; Phosphorylation ; Acetylation
Περίληψη: Nephrolithiasis is a common urinary disorder characterized by high prevalence and recurrence, but the molecular mechanisms underlying calcium oxalate (CaOx)-crystal-induced renal injury remain incompletely understood. We applied integrated proteomic, phosphoproteomic, acetylomic, and lactylomic analyses to kidney tissues from a mouse model of CaOx nephrolithiasis followed by bioinformatic analysis and experimental validation. We identified 658 differentially expressed proteins, 735 differential phosphorylation sites, 335 differential acetylation sites, and 113 differential lactylation sites. Functional enrichment indicated immune activation, fibrotic remodeling, and alterations in PI3K-Akt, NOD-like receptor, p53, and Toll-like receptor signaling together with changes in fatty acid degradation, the tricarboxylic acid cycle, and glycolysis. Kinase activity prediction suggested the relative activation of multiple cyclin-dependent kinases. Proteins associated with ferroptosis, autophagy, necroptosis, and pyroptosis, including ACSL4, BNIP3, RIPK3, and GSDMD, showed coordinated abundance and modification changes. Several candidate sites, including MTOR_S1849, GCLM_K94, GCLM_S59, and GSS_K172, were also dysregulated. These data provide a multiomics resource for CaOx nephrolithiasis and identify candidate PTM events and regulatory pathways for future mechanistic validation.
(© 2026 The Authors. Published by American Chemical Society.)
Grant Information: LHXM2023ZD12004 to Y.N. Shandong Provincial Third Hospital Research Fund
Contributed Indexing: Keywords: acetylomics; ferroptosis; lactylomics; nephrolithiasis; phosphomics; proteomics
SCR Disease Name: Nephrolithiasis, Calcium Oxalate
Entry Date(s): Date Created: 20260904 Date Completed: 20260904 Latest Revision: 20260909
Update Code: 20260909
DOI: 10.1021/acs.jproteome.6c00230
PMID: 42695885
Βάση Δεδομένων: MEDLINE
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PubType: Academic Journal
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  Data: Comprehensive Landscape of Post-Translational Modification Alterations in Nephrolithiasis Revealing Activation of Multiple Cell Death Pathways.
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  Data: <searchLink fieldCode="AU" term="%22Dong+Y%22">Dong Y</searchLink>; Department of Pharmacy, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Zhang+M%22">Zhang M</searchLink>; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan250012, Shandong, China.; School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao266109, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Xu+Y%22">Xu Y</searchLink>; Department of Urology, The Second Qilu Hospital of Shandong University, Jinan250033, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Zhang+J%22">Zhang J</searchLink>; Department of Urology, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Wang+C%22">Wang C</searchLink>; Center for Translational Medicine Research, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Zhang+X%22">Zhang X</searchLink>; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan250012, Shandong, China.<br /><searchLink fieldCode="AU" term="%22Ni+Y%22">Ni Y</searchLink>; Department of Urology, Shandong Provincial Third Hospital, Shandong University, Jinan250031, Shandong, China.
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  Data: <searchLink fieldCode="JN" term="%22101128775%22">Journal of proteome research</searchLink> [J Proteome Res] 2026 Sep 04; Vol. 25 (9), pp. 4688-4703.
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  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22American+Chemical+Society%22">American Chemical Society </searchLink><i>Country of Publication: </i>United States <i>NLM ID: </i>101128775 <i>Publication Model: </i>Print <i>Cited Medium: </i>Internet <i>ISSN: </i>1535-3907 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2215353893%22">15353893 </searchLink><i>NLM ISO Abbreviation: </i>J Proteome Res <i>Subsets: </i>MEDLINE
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  Data: <i>Original Publication</i>: Washington, D.C. : American Chemical Society, c2002-
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  Data: <searchLink fieldCode="MM" term="%22Nephrolithiasis%22">Nephrolithiasis*</searchLink>/<searchLink fieldCode="MM" term="%22Nephrolithiasis+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Nephrolithiasis%22">Nephrolithiasis*</searchLink>/<searchLink fieldCode="MM" term="%22Nephrolithiasis+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Nephrolithiasis%22">Nephrolithiasis*</searchLink>/<searchLink fieldCode="MM" term="%22Nephrolithiasis+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Nephrolithiasis%22">Nephrolithiasis*</searchLink>/<searchLink fieldCode="MM" term="%22Nephrolithiasis+chemically+induced%22">chemically induced</searchLink> <br /><searchLink fieldCode="MM" term="%22Protein+Processing%2C+Post-Translational%22">Protein Processing, Post-Translational*</searchLink><br /><searchLink fieldCode="MH" term="%22Proteomics%22">Proteomics</searchLink>/<searchLink fieldCode="MH" term="%22Proteomics+methods%22">methods</searchLink> ; <searchLink fieldCode="MH" term="%22Cell+Death%22">Cell Death</searchLink>/<searchLink fieldCode="MH" term="%22Cell+Death+genetics%22">genetics</searchLink> ; <searchLink fieldCode="MH" term="%22Kidney%22">Kidney</searchLink>/<searchLink fieldCode="MH" term="%22Kidney+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Kidney%22">Kidney</searchLink>/<searchLink fieldCode="MH" term="%22Kidney+pathology%22">pathology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%22">Mice</searchLink> ; <searchLink fieldCode="MH" term="%22Signal+Transduction%22">Signal Transduction</searchLink> ; <searchLink fieldCode="MH" term="%22Phosphorylation%22">Phosphorylation</searchLink> ; <searchLink fieldCode="MH" term="%22Acetylation%22">Acetylation</searchLink>
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  Label: Abstract
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  Data: Nephrolithiasis is a common urinary disorder characterized by high prevalence and recurrence, but the molecular mechanisms underlying calcium oxalate (CaOx)-crystal-induced renal injury remain incompletely understood. We applied integrated proteomic, phosphoproteomic, acetylomic, and lactylomic analyses to kidney tissues from a mouse model of CaOx nephrolithiasis followed by bioinformatic analysis and experimental validation. We identified 658 differentially expressed proteins, 735 differential phosphorylation sites, 335 differential acetylation sites, and 113 differential lactylation sites. Functional enrichment indicated immune activation, fibrotic remodeling, and alterations in PI3K-Akt, NOD-like receptor, p53, and Toll-like receptor signaling together with changes in fatty acid degradation, the tricarboxylic acid cycle, and glycolysis. Kinase activity prediction suggested the relative activation of multiple cyclin-dependent kinases. Proteins associated with ferroptosis, autophagy, necroptosis, and pyroptosis, including ACSL4, BNIP3, RIPK3, and GSDMD, showed coordinated abundance and modification changes. Several candidate sites, including MTOR_S1849, GCLM_K94, GCLM_S59, and GSS_K172, were also dysregulated. These data provide a multiomics resource for CaOx nephrolithiasis and identify candidate PTM events and regulatory pathways for future mechanistic validation.<br /> (© 2026 The Authors. Published by American Chemical Society.)
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  Data: LHXM2023ZD12004 to Y.N. Shandong Provincial Third Hospital Research Fund
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  Data: <i>Keywords: </i>acetylomics; ferroptosis; lactylomics; nephrolithiasis; phosphomics; proteomics
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  Data: Nephrolithiasis, Calcium Oxalate
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  Data: <i>Date Created: </i>20260904 <i>Date Completed: </i>20260904 <i>Latest Revision: </i>20260909
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  Data: 10.1021/acs.jproteome.6c00230
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  Data: 42695885
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        Text: English
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        StartPage: 4688
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      – SubjectFull: Proteomics methods
        Type: general
      – SubjectFull: Cell Death genetics
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      – SubjectFull: Kidney metabolism
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      – TitleFull: Comprehensive Landscape of Post-Translational Modification Alterations in Nephrolithiasis Revealing Activation of Multiple Cell Death Pathways.
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