ReviewJournal of applied physiology (Bethesda, Md. : 1985)2013
Epigenetic regulation of muscle phenotype and adaptation: a potential role in COPD muscle dysfunction.
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- A double blind randomized placebo control crossover trial on the effect of dietary nitrate supplementation on exercise tolerance in stable moderate chronic obstructive pulmonary disease.BMC pulmonary medicine · 2015Trial
- Review
- Decoding LncRNA in COPD: Unveiling Prognostic and Diagnostic Power and Their Driving Role in Lung Cancer Progression.International journal of molecular sciences · 2024Review
- Mitochondrial quality control: a pathophysiological mechanism and potential therapeutic target for chronic obstructive pulmonary disease.Frontiers in pharmacology · 2024Review
- 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
- Impact of Physical Activity and Exercise on the Epigenome in Skeletal Muscle and Effects on Systemic Metabolism.Biomedicines · 2022Review
- The role of muscle-specific MicroRNAs in patients with chronic obstructive pulmonary disease and skeletal muscle dysfunction.Frontiers in physiology · 2022Review
- Hypercapnic Respiratory Failure-Driven Skeletal Muscle Dysfunction: It Is Time for Animal Model-Based Mechanistic Research.Advances in experimental medicine and biology · 2021Review
- High COAmerican journal of respiratory cell and molecular biology · 2020Article
- Physical Exercise and Epigenetic Modifications in Skeletal Muscle.Sports medicine (Auckland, N.Z.) · 2019Review
- Muscle atrophy in chronic obstructive pulmonary disease: molecular basis and potential therapeutic targets.Journal of thoracic disease · 2018Review
- Exosomes as Mediators of the Systemic Adaptations to Endurance Exercise.Cold Spring Harbor perspectives in medicine · 2018Review
- Muscle hypertrophy in hypoxia with inflammation is controlled by bromodomain and extra-terminal domain proteins.Scientific reports · 2017Article
- Metabolism and Skeletal Muscle Homeostasis in Lung Disease.American journal of respiratory cell and molecular biology · 2017Review
- Molecular and biological pathways of skeletal muscle dysfunction in chronic obstructive pulmonary disease.Chronic respiratory disease · 2016Review
- Article
- The COPD Knowledge Base: enabling data analysis and computational simulation in translational COPD research.Journal of translational medicine · 2014Article
- Beyond the genome: epigenetic mechanisms in lung remodeling.Physiology (Bethesda, Md.) · 2014Review
- Epigenetic mechanisms in respiratory muscle dysfunction of patients with chronic obstructive pulmonary disease.PloS one · 2014Article
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 2 institutions in 2 countries.
Funding
Abstract
Quadriceps muscle dysfunction occurs in one-third of patients with chronic obstructive pulmonary disease (COPD) in very early stages of their condition, even prior to the development of airway obstruction. Among several factors, deconditioning and muscle mass loss are the most relevant contributing factors leading to this dysfunction. Moreover, epigenetics, defined as the process whereby gene expression is regulated by heritable mechanisms that do not affect DNA sequence, could be involved in the susceptibility to muscle dysfunction, pathogenesis, and progression. Herein, we review the role of epigenetic mechanisms in muscle development and adaptation to environmental factors such as immobilization and exercise, and their implications in the pathophysiology and susceptibility to muscle dysfunction in COPD. The epigenetic modifications identified so far include DNA methylation, histone acetylation and methylation, and non-coding RNAs such as microRNAs (miRNAs). In the present review, we describe the specific contribution of epigenetic mechanisms to the regulation of embryonic myogenesis, muscle structure and metabolism, immobilization, and exercise, and in muscles of COPD patients. Events related to muscle development and regeneration and the response to exercise and immobilization are tightly regulated by epigenetic mechanisms. These environmental factors play a key role in the outcome of muscle mass and function as well as in the susceptibility to muscle dysfunction in COPD. Future research remains to be done to shed light on the specific target pathways of miRNA function and other epigenetic mechanisms in the susceptibility, pathogenesis, and progression of COPD muscle dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
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.