Declined expressions of vast mitochondria-related genes represented by CYCS and transcription factor ESRRA in skeletal muscle aging.

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Tytuł:: Declined expressions of vast mitochondria-related genes represented by CYCS and transcription factor ESRRA in skeletal muscle aging.
Autorzy:: Kan J; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Hu Y; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ge Y; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhang W; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lu S; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhao C; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhang R; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liu Y; Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.; Department of Medical Informatics, School of Biomedical Engineering and Informatics, Nanjing Medical University, Nanjing, China.
Źródło:: Bioengineered [Bioengineered] 2021 Dec; Vol. 12 (1), pp. 3485-3502.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Austin : Landes Bioscience
MeSH Terms:: Aging/*genetics
Cytochromes c/*genetics
Mitochondria/*genetics
Muscle, Skeletal/*metabolism
Receptors, Estrogen/*genetics
Adolescent ; Adult ; Aged ; Aging/metabolism ; Child ; Cytochromes c/metabolism ; Humans ; Middle Aged ; Protein Interaction Maps/genetics ; Receptors, Estrogen/metabolism ; Transcriptome/genetics ; Young Adult ; ERRalpha Estrogen-Related Receptor
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Contributed Indexing:: Keywords: CYCS; ESRRA; Skeletal muscle aging; gene expression; mitochondria
Substance Nomenclature:: 0 (Receptors, Estrogen)
9007-43-6 (Cytochromes c)
Entry Date(s):: Date Created: 20210707 Date Completed: 20211217 Latest Revision: 20231213
Update Code:: 20240105
PubMed Central ID:: PMC8806411
DOI:: 10.1080/21655979.2021.1948951
PMID:: 34229541
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Age-related skeletal muscle deterioration (sarcopenia) has a significant effect on the elderly's health and quality of life, but the molecular and gene regulatory mechanisms remain largely unknown. It is necessary to identify the candidate genes related to skeletal muscle aging and prospective therapeutic targets for effective treatments. The age-line-related genes (ALRGs) and age-line-related transcripts (ALRTs) were investigated using the gene expression profiles of GSE47881 and GSE118825 from the Gene Expression Omnibus (GEO) database. The protein-protein interaction (PPI) networks were performed to identify the key molecules with Cytoscape, and Gene Set Enrichment Analysis (GSEA) was used to clarify the potential molecular functions. Two hub molecules were finally obtained and verified with quantitative real-time PCR (qRT-PCR). The results showed that the expression of mitochondria genes involved in mitochondrial electron transport, complex assembly of the respiratory chain, tricarboxylic acid cycle, oxidative phosphorylation, and ATP synthesis were down-regulated in skeletal muscle with aging. We further identified a primary hub gene of CYCS (Cytochrome C) and a key transcription factor of ESRRA (Estrogen-related Receptor Alpha) to be associated closely with skeletal muscle aging. PCR analysis confirmed the expressions of CYCS and ESRRA in gastrocnemius muscles of mice of different ages were significantly different, and decreased gradually with age. In conclusion, the main cause of skeletal muscle aging may be the systematically reduced expression of mitochondrial functional genes. The CYCS and ESRRA may play significant roles in the progression of skeletal muscle aging and serve as potential biomarkers for future diagnosis and treatment.

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