ArticleHuman cell2022
Blockade of ASIC1a inhibits acid-induced rat articular chondrocyte senescence through regulation of autophagy.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- Biological functions and clinical implications of the CMPK2 across multisystemic diseases.Cell & bioscience · 2025Review
- New insights into the role of cellular senescence and rheumatic diseases.Frontiers in immunology · 2025Review
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Ion channels in osteoarthritis: emerging roles and potential targets.Nature reviews. Rheumatology · 2024Review
- P53: A Key Target in the Development of Osteoarthritis.Molecular biotechnology · 2024Review
- Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Acid-sensitive ion channel 1a (ASIC1a), which is abundant in chondrocytes, can sense changes in extracellular acidification. Our previous data demonstrated that ASIC1a is involved in acid-induced rat articular chondrocyte damage in osteoarthritis; however, its specific mechanisms remain unclear. The present study aims to explore the role of ASIC1a in rat articular chondrocyte senescence. RNA-seq transcriptome analysis identified senescence-associated secretory phenotype and matrix metalloproteinases genes were overexpressed by extracellular acidification (pH 6.0) in rat articular chondrocytes. An increase in senescence-associated β-galactosidase and senescence-related markers p16, p21 and p53 was observed in the pH 6.0-treated group compared with the control group. Acid-induced senescence-related markers could be blocked by the ASIC1a-specific inhibitor psalmotoxin-1 in rat articular chondrocytes and human immortalized C28/I2 chondrocyte cell lines. Moreover, our results showed that extracellular acidification increased autophagosomes and the autophagy-related proteins LC3B-II and Beclin-1; these effects could also be reversed by psalmotoxin-1 treatment, indicating ASIC1a participated in acid-induced chondrocyte autophagy. Blocking ASIC1a-mediated autophagy with chloroquine also inhibited senescence-related markers, decreased ROS expression, and restored cell membrane potential induced by pH 6.0 treatment. Taken together, these findings suggested that ASIC1a may be involved in acid-induced rat articular chondrocyte senescence by activating autophagy, which provides a potential therapeutic strategy for the treatment of osteoarthritis.
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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.