Testosterone deficiency caused by castration modulates mitochondrial biogenesis through the Ar/Pgc1α/Tfam pathway
Open accessAbstract
Mammalian mitochondrial biogenesis is a complex process involving mitochondrial proliferation and differentiation. Mitochondrial DNA transcription factor A (TFAM), which encodes a major component of a protein-mitochondrial DNA (mtDNA) complex, is regulated by peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α). Testosterone is the primary male sex hormone and plays an increasingly important role in mammalian development through its interaction with androgen receptor (AR). However, the function of AR in mitochondrial biogenesis induced by testosterone deficiency has not been investigated. Here we explored the molecular mechanism underlying the effect of testosterone deficiency on mitochondrial biogenesis using a Yorkshire boar model. Testosterone deficiency caused by castration induced changes in mtDNA copy numbers in various tissues, and AR showed the opposite tendency to that of mtDNA copy number, particularly in adipose tissues and muscle tissues. In addition, castration weakened the correlation of PGC1α and mtDNA copy number, while AR and TFAM showed a relatively high correlation in both control and castrated pigs. Furthermore, luciferase assays revealed that AR binds to potential AR elements in the TFAM promoter to promote TFAM expression. Taken together, testosterone may be involved in the pathway linking PGC1α to mitochondrial biogenesis through the interaction between AR and TFAM.
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Castration leads to a decrease in mtDNA copy number in the skeletal muscle of male pigs, suggesting that testosterone is required to maintain mitochondrial copy number.
“Castration leads to a decrease in mtDNA copy number in the skeletal muscle of male pigs, suggesting that testosterone is required to maintain mitochondrial copy number (146).”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [146]
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References 63 · Cited by 34
- Authors
- Liu, C., Ma, J., Zhang, J., Zhao, H., Zhu, Y., Qi, J., Liu, L., Zhu, L., Jiang, Y., Tang, G., Li, X., & Li, M.
- Affiliations
- Sichuan Agricultural University (CN)
- Corresponding author
- Li, Mingzhou
- Venue
- Frontiers in Genetics
- Publisher
- Frontiers Media SA
- Published
- 2019-05-29
- Volume
- 10
- Pages
- 505-505
- ISSN
- 1664-8021 (ISSN-L)
- PMC
- PMC6548818
- OpenAlex
- W2945253045
- Cited by
- 34
- References
- 63
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 7 · 2023: 6 · 2022: 5 · 2021: 4 · 2020: 3
- FWCI
- 0.99
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (31601918, CARS-35-01A, CARS 35, 31530073, 31772576)
- Earmarked Fund for China Agriculture Research System (CARS-35-01A, CARS-35, No. CARS-35-01A)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- androgen deficiency, castration, mitochondrial biogenesis, androgen receptor, PGC-1α, TFAM, mitochondrial DNA copy number, adipose tissue, skeletal muscle, Yorkshire boars, androgens
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