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Related Experiment Video

Updated: Nov 9, 2025

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

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Glucose-induced decrease of cystathionine β-synthase mediates renal injuries.

Yanting Yu1,2, Leijuan Xiao1, Zhiyun Ren2

  • 1Department of Nephrology, Nanjing BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 17, 2021
PubMed
Summary
This summary is machine-generated.

Endogenous hydrogen sulfide (H2S) production, specifically cystathionine β-synthase (CBS), is reduced in diabetic kidney disease. This reduction contributes to kidney injury, but H2S donors may offer protection.

Keywords:
cystathionine β-synthasediabetic kidney diseaseglucosehydrogen sulfideproteasomeubiquitination

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Area of Science:

  • Nephrology
  • Biochemistry
  • Molecular Biology

Background:

  • Exogenous hydrogen sulfide (H2S) demonstrates protective effects on kidneys against diabetic injuries in animal models.
  • The role of endogenous H2S in diabetic nephropathy remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of endogenous H2S-producing enzymes in diabetic nephropathy.
  • To determine the mechanisms underlying the reduction of H2S in diabetic kidneys.

Main Methods:

  • Assessed H2S levels, cystathionine β-synthase (CBS) expression, and activity in diabetic mice and cultured mouse renal proximal convoluted tubule (PCT) cells.
  • Utilized siRNA to silence CBS and employed proteasome inhibitor MG132 to investigate degradation pathways.
  • Administered H2S donor GYY4137 to evaluate its protective effects in vivo and in vitro.

Main Results:

  • Diabetic mice exhibited decreased blood and kidney H2S levels, with selective reduction in renal CBS.
  • High glucose reduced CBS protein and activity in PCT cells, increasing CBS ubiquitination and proteasomal degradation.
  • CBS silencing or high glucose increased nitrotyrosine (oxidative stress marker), which was reversed by GYY4137.
  • GYY4137 treatment ameliorated albuminuria and renal damage in diabetic mice.

Conclusions:

  • High glucose reduces renal CBS protein and activity, contributing to diabetic kidney disease pathogenesis.
  • The reduction in CBS and subsequent oxidative injury can be mitigated by H2S supplementation.
  • Endogenous H2S, via CBS, plays a critical role in protecting kidneys from high glucose-induced damage.