ArticleJournal of cachexia, sarcopenia and muscle2018
Cathepsin K activity controls cardiotoxin-induced skeletal muscle repair in mice.
Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Neuromuscular Electrical Stimulation to Combat Muscle Atrophy During Spaceflight: A Narrative Review of Mechanisms and Potential Applications.Life (Basel, Switzerland) · 2026Review
- A Comparative Analysis of Grip Strength Evaluation Methods in a Large Cohort of Aged Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Cathepsins: Emerging targets in the tumor ecosystem to overcome cancers.Seminars in cancer biology · 2025Review
- Antcin K ameliorates cardiotoxin-induced skeletal muscle injury and inflammation via IL-10 regulation.International journal of biological sciences · 2025Article
- Comparative proteomics and micro-RNA analysis of skeletal muscle cell small extracellular vesicles - Unique profiles in cells from severely obese individuals with type 2 diabetesFrontiers in physiology · 2025Article
- Circulatory cathepsin K as biomarkers in older adults with sarcopenia: a case-control study.Frontiers in medicine · 2025Article
- Effect ofDentistry journal · 2024Article
- Degradative Signaling in ATG7-Deficient Skeletal Muscle Following Cardiotoxin Injury.Muscles (Basel, Switzerland) · 2023Article
- Cathepsin S activity controls chronic stress-induced muscle atrophy and dysfunction in mice.Cellular and molecular life sciences : CMLS · 2023Article
- Young bone marrow transplantation prevents aging-related muscle atrophy in a senescence-accelerated mouse prone 10 model.Journal of cachexia, sarcopenia and muscle · 2022Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Article
- Human umbilical cord-derived mesenchymal stromal cells ameliorate aging-associated skeletal muscle atrophy and dysfunction by modulating apoptosis and mitochondrial damage in SAMP10 mice.Stem cell research & therapy · 2022Article
- Cathepsin K activity controls cachexia-induced muscle atrophy via the modulation of IRS1 ubiquitination.Journal of cachexia, sarcopenia and muscle · 2022Article
- Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3.Yonsei medical journal · 2022Article
- Dipeptidyl peptidase-4 inhibition prevents lung injury in mice under chronic stress via the modulation of oxidative stress and inflammation.Experimental animals · 2021Article
- Article
- Proliferin-1 Ameliorates Cardiotoxin-Related Skeletal Muscle Repair in Mice.Stem cells international · 2021Article
- Status of Asp29 and Asp40 in the Interaction ofToxins · 2020Article
- Palmitoyl Protein Thioesterase 1 Is Essential for Myogenic Autophagy of C2C12 Skeletal Myoblast.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCathepsin K (CatK) is a widely expressed cysteine protease that has gained attention because of its enzymatic and non-enzymatic functions in signalling. Here, we examined whether CatK-deficiency (CatK
methodsCardiotoxin (CTX, 20 μM/200 μL) was injected into the left gastrocnemius muscle of male wild-type (CatK
resultsOn post-injection Day 14, CatK deletion ameliorated muscle interstitial fibrosis and remodelling and performance. At an early time point (Day 3), CatK
conclusionsThese results demonstrate that CatK plays an essential role in skeletal muscle loss and fibrosis in response to CTX injury, possibly via a reduction of inflammation and cell apoptosis, suggesting a novel therapeutic strategy for the control of skeletal muscle diseases by regulating CatK activity.
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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.