ArticleBMC musculoskeletal disorders2021
P2Y2 promotes fibroblasts activation and skeletal muscle fibrosis through AKT, ERK, and PKC.
Article in BMC musculoskeletal disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Interaction between purinergic signalling and purinergic modulators with skin wound repair effectors: a systematic review of preclinical in vivo models.Purinergic signalling · 2026Pooled it
- The Piezo1-Ca2+-PI3k/Akt signaling axis as a context-dependent mechanotransduction node during skin wound healing.iScience · 2026Review
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Transcription factor MITF regulates masseter muscle growth and development.Physiological reports · 2025Article
- Long noncoding RNA MALAT1 as a ceRNA drives mouse fibroblast activation via the miR-335-3p/P2ry2 axis.PloS one · 2024Article
- Energy Regulation in Inflammatory Sarcopenia by the Purinergic System.International journal of molecular sciences · 2023Review
- Article
- Therapeutic potential for P2YPurinergic signalling · 2023Review
- Absence of P2YFrontiers in endocrinology · 2022Article
- Role of the Purinergic P2Y2 Receptor in Pulmonary Hypertension.International journal of environmental research and public health · 2021Review
- Fibro-adipogenic progenitors enhance functional and structural properties of human 3D tissue engineered skeletal muscles.Journal of tissue engineeringArticle
- Inhibition of P2Y2 Attenuates Cisplatin-Induced AKI via Reduced Oxidative Stress, Inflammation and Cell Death.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSkeletal muscle atrophy and fibrosis are pathological conditions that contribute to morbidity in numerous conditions including aging, cachexia, and denervation. Muscle atrophy is characterized as reduction of muscle fiber size and loss of muscle mass while muscle fibrosis is due to fibroblasts activation and excessive production of extracellular matrix. Purinergic receptor P2Y2 has been implicated in fibrosis. This study aims to elucidate the roles of P2Y2 in sleketal muscle atrophy and fibrosis.
methodsPrimary muscle fibroblasts were isolated from wild type and P2Y2 knockout (KO) mice and their proliferating and migrating abilities were assessed by CCK-8 and Transwell migration assays respectively. Fibroblasts were activated with TGF-β1 and assessed by western blot of myofibroblast markers including α-SMA, CTGF, and collagen I. Muscle atrophy and fibrosis were induced by transection of distal sciatic nerve and assessed using Masson staining.
resultsP2Y2 KO fibroblasts proliferated and migrated significantly slower than WT fibroblasts with or without TGF-β1.The proliferation and ECM production were enhanced by P2Y2 agonist PSB-1114 and inhibited by antagonist AR-C118925. TGF-β1 induced fibrotic activation was abolished by P2Y2 ablation and inhibited by AKT, ERK, and PKC inhibitors. Ablation of P2Y2 reduced denervation induced muscle atrophy and fibrosis.
conclusionsP2Y2 is a promoter of skeletal muscle atrophy and activation of fibroblasts after muscle injury, which signaling through AKT, ERK and PKC. P2Y2 could be a potential intervention target after muscle injury.
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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.