ArticleRedox biology2018
Homocysteine causes dysfunction of chondrocytes and oxidative stress through repression of SIRT1/AMPK pathway: A possible link between hyperhomocysteinemia and osteoarthritis.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Comparative evaluation of oxidative stress biomarkers F2-isoprostanes and 8-OHdG in Parkinson's disease and Type 2 Diabetes Mellitus: a systematic review and meta-analysis of human studies.Annals of medicine · 2026Pooled it
- Folate deficiency and total shoulder arthroplasty outcomes.Shoulder & elbow · 2026Article
- Homocysteine and mitophagy in diabetic retinopathy: unraveling the underlying molecular crosstalk.Endocrine · 2026Review
- Dual role of homocysteine in enhancing metabolic activity and suppressing inflammatory cytokines in murine immune cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Metformin as an Innate Immune Modulator: Metabolic and Epigenetic Reprogramming of Innate Immune Cells and Therapeutic Implications.Current issues in molecular biology · 2026Review
- SIRT1 regulates CaOx crystal-induced exacerbation of renal mitochondrial dysfunction and fibrosis through PPAR-α in aged mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Gene Polymorphisms Associated with Osteoarthritis: Potential Implications for Nutrigenetics and Precision Nutrition.Nutrients · 2026Review
- Homocysteine as a biomarker in arthritis and depression: Evidence from NHANES and gene expression studies.SAGE open medicine · 2026Article
- Energy crisis and cartilage collapse: metabolic reprogramming of chondrocytes in osteoarthritis.Frontiers in immunology · 2026Review
- The causal role of homocysteine in multiple diseases: a systematic review of Mendelian randomization studies.Nutrition & metabolism · 2025Review
- Metabolic Reprogramming in Stromal and Immune Cells in Rheumatoid Arthritis and Osteoarthritis: Therapeutic Possibilities.European journal of immunology · 2025Review
- Gut microbiota and blood biomarkers in IBD-Related arthritis: insights from mendelian randomization.Scientific reports · 2025Article
- Mesoporous Prussian blue nanoparticle neuroconduit for the biological therapy targeting oxidative stress reduction, inflammation inhibition, and nerve regeneration.Journal of nanobiotechnology · 2025Article
- AMPK signaling in osteoarthritis: from mechanisms to targeted therapeutics.Frontiers in pharmacology · 2025Review
- Integrative in-silico and in-vitro analysis of taurine and vitamin B12 in modulating PPARγ and Wnt signaling in hyperhomocysteinemia-induced osteoporosis.Biology direct · 2024Article
- Preparing the soil: Adjusting the metabolic health of patients with chronic wounds and musculoskeletal diseases.International wound journal · 2024Review
- Latest Advances in Chondrocyte-Based Cartilage Repair.Biomedicines · 2024Review
- The role and intervention of mitochondrial metabolism in osteoarthritis.Molecular and cellular biochemistry · 2024Review
- Middle aged CAMKII-Cre:CbsExperimental animals · 2024Article
- Therapeutic potential of hydrogen sulfide in osteoarthritis development.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has indicated that the perturbed expression of homocysteine (Hcy) may induce mitochondrial dysfunction and disturb bone metabolism. Sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK) are two critical sensors that regulate mitochondrial biogenesis and have been recognized as therapeutic targets in osteoarthritis (OA). This study was designed to test whether Hcy caused pro-osteoarthritic changes through modulation of SIRT1 and AMPK. Our results showed that administration of Hcy reduced the SIRT1/AMPK/PGC-1α signaling in chondrocytes, leading to mitochondrial dysfunction as a result of increased oxidative stress and apoptosis. Moreover, we demonstrated that the expression of NF-κB, COX-2, IL-8, and MMP-13 were elevated subsequent to inhibition of SIRT1/AMPK/PGC-1α/PPAR-γ pathway by homocysteine, thereby causing detrimental effects on chondrocytes. In the animal model of diet-induced hyperhomocysteinemia (HHcy), we observed the similar findings that SIRT1/PGC-1α/PPAR-γ cascades were downregulated with elevated MMP-13 and COX-2. Taken together, data from the current study revealed that the reduced SIRT1 by Hcy may contribute to degradative cartilage process, which provided insight into the etiology of OA.
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