ArticleAdvances in experimental medicine and biology2017
Redox-Dependent Calpain Signaling in Airway and Pulmonary Vascular Remodeling in COPD.
Article in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Proteomic analysis of lung responses to SARS-CoV-2 infection in aged non-human primates: clinical and research relevance.GeroScience · 2024Article
- PI3K/AKT/FOXO3a Pathway Induces Muscle Atrophy by Ubiquitin-Proteasome System and Autophagy System in COPD Rat Model.Cell biochemistry and biophysics · 2024Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- CAPN5 attenuates cigarette smoke extract-induced apoptosis and inflammation in BEAS-2B cells.Tobacco induced diseases · 2024Article
- The Correlation of Serum Calpain 1 Activity and Concentrations of Interleukin 33 in COVID-19 Acute Respiratory Distress Syndrome.Biomedicines · 2023Article
- HDAC6 Activates ERK in Airway and Pulmonary Vascular Remodeling of Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2021Article
- Reactive Oxygen Species-Dependent Calpain Activation Contributes to Airway and Pulmonary Vascular Remodeling in Chronic Obstructive Pulmonary Disease.Antioxidants & redox signaling · 2019Article
- Oligonucleotide Microarrays Identified Potential Regulatory Genes Related to Early Outward Arterial Remodeling Induced by Tissue Plasminogen Activator.Frontiers in physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The calcium-dependent cytosolic, neutral, thiol endopeptidases, calpains, perform limited cleavage of their substrates thereby irreversibly changing their functions. Calpains have been shown to be involved in several physiological processes such as cell motility, proliferation, cell cycle, signal transduction, and apoptosis. Overactivation of calpain or mutations in the calpain genes contribute to a number of pathological conditions including neurodegenerative disorders, rheumatoid arthritis, cancer, and lung diseases. High concentrations of reactive oxygen and nitrogen species (RONS) originated from cigarette smoke or released by numerous cell types such as activated inflammatory cells and other respiratory cells cause oxidative and nitrosative stress contributing to the pathogenesis of COPD. RONS and calpain play important roles in the development of airway and pulmonary vascular remodeling in COPD. Published data show that increased RONS production is associated with increased calpain activation and/or elevated calpain protein level, leading to epithelial or endothelial barrier dysfunction, neovascularization, lung inflammation, increased smooth muscle cell proliferation, and deposition of extracellular matrix protein. Further investigation of the redox-dependent calpain signaling may provide future targets for the prevention and treatment of COPD.
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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.