ArticleInternational journal of biological sciences2017
Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.
Article in International journal of biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Metabolomics approaches for the early detection and therapeutics: type 2 diabetes-induced diabetic kidney disease-a systematic review and meta-analysis.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- The Links between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling-A Systematic Review.Toxins · 2020Pooled it
- Disease landscape-guided design of neutrophil-specific reporters for early and accurate pneumonia detection in vivo and in urine.Science advances · 2026Article
- The prognostic value of hyperhomocysteinemia in IgA nephropathy.International urology and nephrology · 2026Article
- Interplay between gut microbiota and acute kidney injury: a review of their mutual influence and causation.Renal failure · 2025Review
- Differential Effects of High Methionine Diet on Biochemical Parameters in Normal and Diabetic Rat Models.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2025Article
- SMYD2 Promotes Renal Tubular Cell Apoptosis and Chronic Kidney Disease Following Cisplatin Nephrotoxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Targeting Endoplasmic Reticulum Stress by Natural and Chemical Compounds Ameliorates Cisplatin-Induced Nephrotoxicity: A Review.Biological trace element research · 2025Review
- Multifaceted therapeutic potentials of catalpol, an iridoid glycoside: an updated comprehensive review.Inflammopharmacology · 2025Review
- Cisplatin Nephrotoxicity Is Critically Mediated by the Availability of BECLIN1.International journal of molecular sciences · 2024Article
- Review
- Numb Promotes Autophagy through p53 Pathway in Acute Kidney Injury Induced by Cisplatin.Analytical cellular pathology (Amsterdam) · 2022Article
- Aberrant Expression of Mitochondrial SAM Transporter SLC25A26 Impairs Oocyte Maturation and Early Development in Mice.Oxidative medicine and cellular longevity · 2022Article
- Hyperhomocysteinemia exacerbates acute kidney injuryFrontiers in physiology · 2022Article
- Review
- Review
- Hyperhomocysteinemia exacerbates ischemia-reperfusion injury-induced acute kidney injury by mediating oxidative stress, DNA damage, JNK pathway, and apoptosis.Open life sciences · 2021Article
- Compound C Protects Against Cisplatin-Induced Nephrotoxicity Through Pleiotropic Effects.Frontiers in physiology · 2020Article
- Integrated Analysis of m6A Methylome in Cisplatin-Induced Acute Kidney Injury and Berberine Alleviation in Mouse.Frontiers in genetics · 2020Article
- Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperhomocysteinemia (HHcy) has been linked to several clinical manifestations including chronic kidney disease. However, it is not known whether HHcy has a role in the development of acute kidney injury (AKI). In the present study, we reported that HHcy mice developed more severe renal injury after cisplatin injection and ischemia-reperfusion injury shown as more severe renal tubular damage and higher serum creatinine. In response to cisplatin, HHcy mice showed more prevalent tubular cell apoptosis and decreased tubular cell proliferation. Mechanistically, a heightened ER stress and a reduced Akt activity were observed in kidney tissues of HHcy mice after cisplatin injection. Stimulating cultured NRK-52E cells with Hcy significantly increased the fraction of cells in G2/M phase and cell apoptosis together with decreased Akt kinase activity. Akt agonist IGF-1 rescued HHcy-induced cell cycle arrest and cell apoptosis. In conclusion, the present study provides evidence that HHcy increases the sensitivity and severity of AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.