Posters
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Medical Student
Academic Level (Author 3)
Faculty
Discipline/Specialty (Author 3)
Neuroscience
Discipline Track
Biomedical Science
Abstract
Background: In 2020, it was estimated that there were over 480 million cases of chronic obstructive pulmonary disease (COPD) worldwide. Up to 40% of COPD patients suffer from a certain degree of muscle atrophy. The severity of this muscle atrophy is normally correlated with an increased mortality rate among these patients. The goal of this study is to underline the causes of muscle atrophy/dysfunction in the COPD population and to investigate treatment options.
Methods: We conducted an extensive literature review using the PubMed database, mainly focusing on publications from 2013 to 2024. Our objective was to identify the biological mechanisms underlying muscle atrophy and dysfunction in COPD patients. Additionally, we aimed to explore potential management and treatment strategies that could be employed to improve patient outcomes. This comprehensive review allowed us to synthesize current knowledge on the topic and highlight emerging therapeutic approaches that may mitigate the adverse effects of muscle atrophy in individuals with COPD.
Results: Through our review of the body of research, we were able to find that muscle atrophy in COPD patients is a multifactorial issue. The muscle atrophy that occurs is not only a result of COPD pathophysiology itself, but also because of treatments, limitations brought about by COPD, and by comorbidities that frequently appear in COPD patients. Through our review of the scientific literature, we saw that as many as 98% of COPD patients have at least one comorbidity. This makes studying COPD in isolation difficult in the general population because of the prevalence of comorbidities. Using animal models, researchers can induce COPD to study the effects that it has without confounding factors. We were able to find that there are multiple biological mechanisms that cause muscle dysfunction/atrophy in COPD patients. We also looked at the possible interventions for the treatment of muscle atrophy. The interventions consisted of implementing strength training, structured nutritional programs, anabolic steroids to combat muscle loss, and various other interventions that interfere with metabolic pathways that lead to muscle atrophy in COPD.
Conclusion: Muscle atrophy in COPD is not merely a consequence of the condition and its associated comorbidities. It is also driven by the activation of distinct metabolic pathways in response to the hypoxia induced by COPD. Several studies have concentrated on specific pathways contributing to muscle atrophy and have proposed potential treatments to address this issue. Most of the research performed has demonstrated that these treatments are expected to reduce the muscle atrophy seen in COPD as well as decrease the burden of the disease.
Presentation Type
Poster
Recommended Citation
Mills, Justin D.; Garcia, Hiram L.; and Zuo, Alex, "New Insights into the Mechanisms of Skeletal Muscle Atrophy in COPD" (2024). Research Colloquium. 71.
https://scholarworks.utrgv.edu/colloquium/2024/posters/71
Included in
New Insights into the Mechanisms of Skeletal Muscle Atrophy in COPD
Background: In 2020, it was estimated that there were over 480 million cases of chronic obstructive pulmonary disease (COPD) worldwide. Up to 40% of COPD patients suffer from a certain degree of muscle atrophy. The severity of this muscle atrophy is normally correlated with an increased mortality rate among these patients. The goal of this study is to underline the causes of muscle atrophy/dysfunction in the COPD population and to investigate treatment options.
Methods: We conducted an extensive literature review using the PubMed database, mainly focusing on publications from 2013 to 2024. Our objective was to identify the biological mechanisms underlying muscle atrophy and dysfunction in COPD patients. Additionally, we aimed to explore potential management and treatment strategies that could be employed to improve patient outcomes. This comprehensive review allowed us to synthesize current knowledge on the topic and highlight emerging therapeutic approaches that may mitigate the adverse effects of muscle atrophy in individuals with COPD.
Results: Through our review of the body of research, we were able to find that muscle atrophy in COPD patients is a multifactorial issue. The muscle atrophy that occurs is not only a result of COPD pathophysiology itself, but also because of treatments, limitations brought about by COPD, and by comorbidities that frequently appear in COPD patients. Through our review of the scientific literature, we saw that as many as 98% of COPD patients have at least one comorbidity. This makes studying COPD in isolation difficult in the general population because of the prevalence of comorbidities. Using animal models, researchers can induce COPD to study the effects that it has without confounding factors. We were able to find that there are multiple biological mechanisms that cause muscle dysfunction/atrophy in COPD patients. We also looked at the possible interventions for the treatment of muscle atrophy. The interventions consisted of implementing strength training, structured nutritional programs, anabolic steroids to combat muscle loss, and various other interventions that interfere with metabolic pathways that lead to muscle atrophy in COPD.
Conclusion: Muscle atrophy in COPD is not merely a consequence of the condition and its associated comorbidities. It is also driven by the activation of distinct metabolic pathways in response to the hypoxia induced by COPD. Several studies have concentrated on specific pathways contributing to muscle atrophy and have proposed potential treatments to address this issue. Most of the research performed has demonstrated that these treatments are expected to reduce the muscle atrophy seen in COPD as well as decrease the burden of the disease.