» Articles » PMID: 35892590

Shared and Divergent Epigenetic Mechanisms in Cachexia and Sarcopenia

Overview
Journal Cells
Publisher MDPI
Date 2022 Jul 27
PMID 35892590
Authors
Affiliations
Soon will be listed here.
Abstract

Significant loss of muscle mass may occur in cachexia and sarcopenia, which are major causes of mortality and disability. Cachexia represents a complex multi-organ syndrome associated with cancer and chronic diseases. It is often characterized by body weight loss, inflammation, and muscle and adipose wasting. Progressive muscle loss is also a hallmark of healthy aging, which is emerging worldwide as a main demographic trend. A great challenge for the health care systems is the age-related decline in functionality which threatens the independence and quality of life of elderly people. This biological decline can also be associated with functional muscle loss, known as sarcopenia. Previous studies have shown that microRNAs (miRNAs) play pivotal roles in the development and progression of muscle wasting in both cachexia and sarcopenia. These small non-coding RNAs, often carried in extracellular vesicles, inhibit translation by targeting messenger RNAs, therefore representing potent epigenetic modulators. The molecular mechanisms behind cachexia and sarcopenia, including the expression of specific miRNAs, share common and distinctive trends. The aim of the present review is to compile recent evidence about shared and divergent epigenetic mechanisms, particularly focusing on miRNAs, between cachexia and sarcopenia to understand a facet in the underlying muscle wasting associated with these morbidities and disclose potential therapeutic interventions.

Citing Articles

Body composition characteristics and influencing factors of different parts of sarcopenia in elderly people: A community-based cross-sectional survey.

Dong X, Bi B, Hu Y, Wang L, Liu X, Li W Aging Med (Milton). 2024; 7(3):384-392.

PMID: 38975318 PMC: 11222755. DOI: 10.1002/agm2.12327.


Sarcopenia as a Risk Factor for Alzheimer's Disease: Genetic and Epigenetic Perspectives.

Raleigh S, Orchard K Genes (Basel). 2024; 15(5).

PMID: 38790190 PMC: 11121242. DOI: 10.3390/genes15050561.


Higher systemic immune-inflammation index is associated with sarcopenia in individuals aged 18-59 years: a population-based study.

Zhao J, Zeng L, Liang G, Dou Y, Zhou G, Pan J Sci Rep. 2023; 13(1):22156.

PMID: 38092854 PMC: 10719257. DOI: 10.1038/s41598-023-49658-1.


Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.

Nevi L, Pollanen N, Penna F, Caretti G Int J Mol Sci. 2023; 24(22).

PMID: 38003594 PMC: 10671811. DOI: 10.3390/ijms242216404.


Extracellular vesicles and Duchenne muscular dystrophy pathology: Modulators of disease progression.

Yedigaryan L, Sampaolesi M Front Physiol. 2023; 14:1130063.

PMID: 36891137 PMC: 9987248. DOI: 10.3389/fphys.2023.1130063.

References
1.
Noonan E, Place R, Pookot D, Basak S, Whitson J, Hirata H . miR-449a targets HDAC-1 and induces growth arrest in prostate cancer. Oncogene. 2009; 28(14):1714-24. DOI: 10.1038/onc.2009.19. View

2.
El Amrani M, Vermersch M, Fulbert M, Prodeau M, Lecolle K, Hebbar M . Impact of sarcopenia on outcomes of patients undergoing pancreatectomy: A retrospective analysis of 107 patients. Medicine (Baltimore). 2018; 97(39):e12076. PMC: 6181530. DOI: 10.1097/MD.0000000000012076. View

3.
Di W, Zhang W, Zhu B, Li X, Tang Q, Zhou Y . Colorectal cancer prompted adipose tissue browning and cancer cachexia through transferring exosomal miR-146b-5p. J Cell Physiol. 2020; 236(7):5399-5410. DOI: 10.1002/jcp.30245. View

4.
Van Rooij E, Quiat D, Johnson B, Sutherland L, Qi X, Richardson J . A family of microRNAs encoded by myosin genes governs myosin expression and muscle performance. Dev Cell. 2009; 17(5):662-73. PMC: 2796371. DOI: 10.1016/j.devcel.2009.10.013. View

5.
Faralli H, Wang C, Nakka K, Benyoucef A, Sebastian S, Zhuang L . UTX demethylase activity is required for satellite cell-mediated muscle regeneration. J Clin Invest. 2016; 126(4):1555-65. PMC: 4811158. DOI: 10.1172/JCI83239. View