ArticleMolecular medicine reports2021
Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular mechanisms and treatment strategies for estrogen deficiency-related and glucocorticoid-induced osteoporosis: a comprehensive review.Inflammopharmacology · 2025Review
- Glucosinolates in Human Health: Metabolic Pathways, Bioavailability, and Potential in Chronic Disease Prevention.Foods (Basel, Switzerland) · 2025Review
- Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2025Review
- Targeting Cellular Senescence for Healthy Aging: Advances in Senolytics and Senomorphics.Drug design, development and therapy · 2025Review
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
- Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane.Biomedicines · 2024Review
- Sulforaphane Inhibits IL-1β-Induced IL-6 by Suppressing ROS Production, AP-1, and STAT3 in Colorectal Cancer HT-29 Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Quercetin and dasatinib, two powerful senolytics in age-related cardiovascular disease.Biogerontology · 2024Review
- Challenges in Pharmacological Intervention in Perilipins (PLINs) to Modulate Lipid Droplet Dynamics in Obesity and Cancer.Cancers · 2023Review
- Natural compounds protect against the pathogenesis of osteoarthritis by mediating the NRF2/ARE signaling.Frontiers in pharmacology · 2023Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. Chondrocyte apoptosis is the primary pathogenic mechanism of OA and is considered to be a potential therapeutic target. Sulforaphane (SFN), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti‑apoptotic effect by activating sirtuin 1 (SIRT1). To the best of our knowledge, however, the effects of SFN on apoptotic responses in OA have not been reported. In the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SIRT1 in a H
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