ArticleDiabetes2012
Catalase deficiency accelerates diabetic renal injury through peroxisomal dysfunction.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
93 citing papers in PubMed, 174 citations in OpenAlex.
- USP30-Mediated Deubiquitination of PEX5 Suppresses Pexophagy to Drive Tubular Injury in Diabetic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Pathophysiological Mechanisms of Diabetes-Induced Macrovascular and Microvascular Complications: The Role of Oxidative Stress.Medical sciences (Basel, Switzerland) · 2025Review
- Mitigating renal dysfunction in liver cirrhosis: Therapeutic role of ferrous sulphate, folic acid, and its co-administration.Toxicology reports · 2025Article
- PEX11B palmitoylation couples peroxisomal dysfunction with Schwann cells fail in diabetic neuropathy.Journal of biomedical science · 2025Article
- Peroxisomal homeostasis in metabolic diseases and its implication in ferroptosis.Cell communication and signaling : CCS · 2024Review
- Interplay between the Redox System and Renal Tubular Transport.Antioxidants (Basel, Switzerland) · 2024Review
- Multitarget Pharmacology of Sulfur-Nitrogen Heterocycles: Anticancer and Antioxidant Perspectives.Antioxidants (Basel, Switzerland) · 2024Review
- A Novel Peroxisome-Related Gene Signature Predicts Breast Cancer Prognosis and Correlates with T Cell Suppression.Breast cancer (Dove Medical Press) · 2024Article
- Oxidative Stress Induced by Lipotoxicity and Renal Hypoxia in Diabetic Kidney Disease and Possible Therapeutic Interventions: Targeting the Lipid Metabolism and Hypoxia.Antioxidants (Basel, Switzerland) · 2023Review
- Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease.Nature reviews. Nephrology · 2023Review
- DsbA-L interacting with catalase in peroxisome improves tubular oxidative damage in diabetic nephropathy.Redox biology · 2023Article
- Effect of Organic Selenium on the Homeostasis of Trace Elements, Lipid Peroxidation, and mRNA Expression of Antioxidant Proteins in Mouse Organs.International journal of molecular sciences · 2023Article
- Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections.International journal of molecular sciences · 2023Review
- The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications.Frontiers in endocrinology · 2023Review
- Mouse Models to Study Peroxisomal Functions and Disorders: Overview, Caveats, and Recommendations.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Peroxisomal Fitness: A Potential Protective Mechanism of Fenofibrate against High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice.Diabetes & metabolism journal · 2022Article
- Peroxisomal regulation of energy homeostasis: Effect on obesity and related metabolic disorders.Molecular metabolism · 2022Review
- The multifaceted role of kidney tubule mitochondrial dysfunction in kidney disease development.Trends in cell biology · 2022Review
- Exploring the mechanism of hirudin in the treatment of diabetic kidney disease using network pharmacology combined with molecular docking verification.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial reactive oxygen species (ROS) play an important role in diabetes complications, including diabetic nephropathy (DN). Plasma free fatty acids (FFAs) as well as glucose are increased in diabetes, and peroxisomes and mitochondria participate in FFA oxidation in an interconnected fashion. Therefore, we investigated whether deficiency of catalase, a major peroxisomal antioxidant, accelerates DN through peroxisomal dysfunction and abnormal renal FFA metabolism. Diabetes was induced by multiple injections of low-dose streptozotocin into catalase knock-out (CKO) and wild-type (WT) C57BL/6 mice. Murine mesangial cells (MMCs) transfected with catalase small interfering RNA followed by catalase overexpression were used to further elucidate the role of endogenous catalase. Despite equivalent hyperglycemia, parameters of DN, along with markers of oxidative stress, were more accelerated in diabetic CKO mice than in diabetic WT mice up to 10 weeks of diabetes. CKO mice and MMCs showed impaired peroxisomal/mitochondrial biogenesis and FFA oxidation. Catalase deficiency increased mitochondrial ROS and fibronectin expression in response to FFAs, which were effectively restored by catalase overexpression or N-acetylcysteine. These data provide unprecedented evidence that FFA-induced peroxisomal dysfunction exacerbates DN and that endogenous catalase plays an important role in protecting the kidney from diabetic stress through maintaining peroxisomal and mitochondrial fitness.
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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.