ArticleInternational journal of molecular sciences2022
Urocortin-1 Is Chondroprotective in Response to Acute Cartilage Injury via Modulation of Piezo1.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Roles of Piezo channels in dentofacial deformity: Onset, orthodontic treatment, and associated diseases.Genes & diseases · 2026Review
- Piezo1-mediated mechanotransduction and metabolic regulation in bone health: molecular mechanisms and implications for bone disorders.Frontiers in cell and developmental biology · 2026Review
- Implications of mechanosensitive ion channels in the pathogenesis of osteoarthritis: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- Exploring the Multifactorial Regulation of PIEZO1 in Chondrocytes: Mechanisms and Implications.International journal of medical sciences · 2025Review
- Piezo1 and tissue fibrosis: insights into its role and potential for modulation.Burns & trauma · 2025Review
- The role of mechanosensitive ion channel Piezo1 in knee osteoarthritis inflammation.Channels (Austin, Tex.) · 2024Review
- Piezo1 activation accelerates osteoarthritis progression and the targeted therapy effect of artemisinin.Journal of advanced research · 2024Article
- The chondrocyte "mechanome": Activation of the mechanosensitive ion channels TRPV4 and PIEZO1 drives unique transcriptional signatures.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- The emerging role of Piezo1 in the musculoskeletal system and disease.Theranostics · 2024Review
- Aging Changes the Efficacy of Central Urocortin 2 to Induce Weight Loss in Rats.International journal of molecular sciences · 2023Article
- The role of PIEZO ion channels in the musculoskeletal system.American journal of physiology. Cell physiology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-traumatic OA (PTOA) is often triggered by injurious, high-impact loading events which result in rapid, excessive chondrocyte cell death and a phenotypic shift in residual cells toward a more catabolic state. As such, the identification of a disease-modifying OA drug (DMOAD) that can protect chondrocytes from death following impact injury, and thereby prevent cartilage degradation and progression to PTOA, would offer a novel intervention. We have previously shown that urocortin-1 (Ucn) is an essential endogenous pro-survival factor that protects chondrocytes from OA-associated pro-apoptotic stimuli. Here, using a drop tower PTOA-induction model, we demonstrate the extent of Ucn's chondroprotective role in cartilage explants exposed to excessive impact load. Using pathway-specific agonists and antagonists, we show that Ucn acts to block load-induced intracellular calcium accumulation through blockade of the non-selective cation channel Piezo1 rather than TRPV4. This protective effect is mediated primarily through the Ucn receptor CRF-R1 rather than CRF-R2. Crucially, we demonstrate that the chondroprotective effect of Ucn is maintained whether it is applied pre-impact or post-impact, highlighting the potential of Ucn as a novel DMOAD for the prevention of injurious impact overload-induced PTOA.
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Registered trials
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