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Homocysteine in Chronic Kidney Disease

Elena A Ostrakhovitch1, Siamak Tabibzadeh1

  • 1Frontiers in Bioscience Research Institute in Aging and Cancer, Irvine, California, USA.

Advances in Clinical Chemistry
|October 17, 2015
PubMed

Insights

High homocysteine (Hcy) levels in kidney disease cause oxidative stress and thiol modifications, worsening disease progression. Understanding these redox changes is key to managing chronic kidney disease (CKD).

Area of Science:

  • Biochemistry
  • Nephrology
  • Oxidative Stress Research

Background:

  • Hyperhomocysteinemia is prevalent in chronic and end-stage kidney disease.
  • Elevated homocysteine (Hcy) disrupts cellular redox balance and homeostasis.
  • This leads to significant oxidative stress and thiol modifications.

Purpose of the Study:

  • To review redox regulation mechanisms in chronic kidney disease (CKD).
  • To elucidate how homocysteine-induced cysteinyl modifications contribute to CKD development and progression.
  • To discuss signaling pathways affected by aberrant cysteinyl modifications, focusing on transsulfuration.

Main Methods:

  • Literature review of redox regulation mechanisms.
  • Analysis of homocysteine's role in thiol modifications.
  • Discussion of signaling events and transsulfuration pathways.

Main Results:

  • Excess homocysteine triggers persistent thiol modifications, overwhelming cellular proteostasis.
  • Cysteinyl modifications, including N-homocysteinylation, are key mediators of Hcy-induced damage.
  • Aberrant thiol modifications impact cellular responses and metabolic pathways.

Conclusions:

  • Homocysteine-induced cysteinyl modifications are critical contributors to CKD pathogenesis.
  • Understanding these redox alterations offers insights into CKD progression.
  • Targeting transsulfuration pathways may offer therapeutic strategies for managing CKD.

Keywords:
Cysteine-targeted oxidation/thiolationHomocysteineHydrogen sulfideKidneyPodocytesProtein posttranslation modificationRedox regulationSulfhydrationTranssulfuration pathway

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