ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Exposure to cigarette smoke induces overexpression of von Hippel-Lindau tumor suppressor in mouse skeletal muscle.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- Muscle-lung crosstalk in COPD: how exercise training modulates protein metabolism and inflammation in experimental COPD models.Frontiers in immunology · 2026Review
- Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.International journal of molecular sciences · 2023Review
- Impaired regenerative capacity contributes to skeletal muscle dysfunction in chronic obstructive pulmonary disease.American journal of physiology. Cell physiology · 2022Review
- Review
- Soluble epoxide hydrolase inhibitor can protect the femoral head against tobacco smoke exposure-induced osteonecrosis in spontaneously hypertensive rats.Toxicology · 2022Article
- Integrating Mechanisms of Exacerbated Atrophy and Other Adverse Skeletal Muscle Impact in COPD.Frontiers in physiology · 2022Review
- Article
- Smoking Alters Inflammation and Skeletal Stem and Progenitor Cell Activity During Fracture Healing in Different Murine Strains.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Hypercapnic Respiratory Failure-Driven Skeletal Muscle Dysfunction: It Is Time for Animal Model-Based Mechanistic Research.Advances in experimental medicine and biology · 2021Review
- The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study.BMC pulmonary medicine · 2020Article
- AMP-Activated Protein Kinase (AMPK) at the Crossroads Between COInternational journal of molecular sciences · 2020Review
- IL-13-driven pulmonary emphysema leads to skeletal muscle dysfunction attenuated by endurance exercise.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Hypercapnia-Driven Skeletal Muscle Dysfunction in an Animal Model of Pulmonary Emphysema Suggests a Complex Phenotype.Frontiers in physiology · 2020Article
- Immune-regulating effects of exercise on cigarette smoke-induced inflammation.Journal of inflammation research · 2018Review
- HIF-1-driven skeletal muscle adaptations to chronic hypoxia: molecular insights into muscle physiology.Cellular and molecular life sciences : CMLS · 2015Review
- Recent advances in pre-clinical mouse models of COPD.Clinical science (London, England : 1979) · 2014Review
- Alterations in skeletal muscle cell homeostasis in a mouse model of cigarette smoke exposure.PloS one · 2013Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cigarette smoke (CS) is a well-established risk factor in the development of chronic obstructive pulmonary disease (COPD). In contrast, the extent to which CS exposure contributes to the development of the systemic manifestations of COPD, such as skeletal muscle dysfunction and wasting, remains largely unknown. Decreased skeletal muscle capillarization has been previously reported in early stages of COPD and might play an important role in the development of COPD-associated skeletal muscle abnormalities. To investigate the effects of chronic CS exposure on skeletal muscle capillarization and exercise tolerance, a mouse model of CS exposure was used. The 129/SvJ mice were exposed to CS for 6 mo, and the expression of putative elements of the hypoxia-angiogenic signaling cascade as well as muscle capillarization were studied. Additionally, functional tests assessing exercise tolerance/endurance were performed in mice. Compared with controls, skeletal muscles from CS-exposed mice exhibited significantly enhanced expression of von Hippel-Lindau tumor suppressor (VHL), ubiquitin-conjugating enzyme E2D1 (UBE2D1), and prolyl hydroxylase-2 (PHD2). In contrast, hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression was reduced. Furthermore, reduced muscle fiber cross-sectional area, decreased skeletal muscle capillarization, and reduced exercise tolerance were also observed in CS-exposed animals. Taken together, the current results provide evidence linking chronic CS exposure and induction of VHL expression in skeletal muscles leading toward impaired hypoxia-angiogenesis signal transduction, reduced muscle fiber cross-sectional area, and decreased exercise tolerance.
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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.