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Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
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Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

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Progress in the Mechanism of Hyperhomocysteinemia-Induced Renal Injury

Jin Zhang, Dagong Zhang, Zhen Xu

    Clinical Laboratory
    |December 9, 2025
    PubMed

    Insights

    High homocysteine (Hcy) levels independently increase cardiovascular disease risk. This study details how hyperhomocysteinemia accelerates chronic kidney disease progression through multiple complex mechanisms.

    Area of Science:

    • Nephrology
    • Cardiovascular Medicine
    • Biochemistry

    Background:

    • Homocysteine (Hcy), a methionine metabolism byproduct, is a known cardiovascular disease risk factor.
    • The link between hyperhomocysteinemia and renal disease is increasingly recognized.
    • Mechanisms of Hcy's role in cardiovascular pathology within chronic kidney disease (CKD) are complex.

    Purpose of the Study:

    • To summarize the multifaceted mechanisms by which hyperhomocysteinemia contributes to renal injury.
    • To elucidate the pathways involved in Hcy-induced cardiovascular and renal pathology in CKD patients.

    Main Methods:

    • Comprehensive literature review and synthesis.
    • Analysis of existing research on hyperhomocysteinemia and kidney disease.

    Main Results:

    • Hyperhomocysteinemia induces renal injury via oxidative stress, endothelial damage, inflammation, autophagy, apoptosis, fibrosis, and epigenetic changes.
    • These pathways synergistically contribute to glomerulosclerosis, tubular atrophy, and interstitial fibrosis.
    • Multiple interrelated mechanisms accelerate renal failure in hyperhomocysteinemic individuals.

    Conclusions:

    • Hyperhomocysteinemia exacerbates renal damage through a complex interplay of pathways.
    • Targeting these multiple mechanisms may be crucial for comprehensive intervention strategies.
    • Effective management of hyperhomocysteinemia is vital for slowing CKD progression and preventing renal failure.
    Abstract

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