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Hypoxia induces PGC-1α expression and mitochondrial biogenesis in the myocardium of TOF patients.
Cell Res. 2010 Jun; 20(6):676-87.CR

Abstract

PGC-1alpha, a potent transcriptional coactivator, is the major regulator of mitochondrial biogenesis and activity in the cardiac muscle. The dysregulation of PGC-1alpha and its target genes has been reported to be associated with congenital and acquired heart diseases. By examining myocardium samples from patients with Tetralogy of Fallot, we show here that PGC-1alpha expression levels are markedly increased in patients compared with healthy controls and positively correlated with the severity of cyanosis. Furthermore, hypoxia significantly induced the expression of PGC-1alpha and mitochondrial biogenesis in cultured cardiac myocytes. Mechanistic studies suggest that hypoxia-induced PGC-1alpha expression is regulated through the AMPK signaling pathway. Together, our data indicate that hypoxia can stimulate the expression of PGC-1alpha and mitochondrial biogenesis in the cardiac myocytes, and this process might provide a potential adaptive mechanism for cardiac myocytes to increase ATP output and minimize hypoxic damage to the heart.

Authors+Show Affiliations

Jiangsu Diabetes Center, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20368732

Citation

Zhu, Lingyun, et al. "Hypoxia Induces PGC-1α Expression and Mitochondrial Biogenesis in the Myocardium of TOF Patients." Cell Research, vol. 20, no. 6, 2010, pp. 676-87.
Zhu L, Wang Q, Zhang L, et al. Hypoxia induces PGC-1α expression and mitochondrial biogenesis in the myocardium of TOF patients. Cell Res. 2010;20(6):676-87.
Zhu, L., Wang, Q., Zhang, L., Fang, Z., Zhao, F., Lv, Z., Gu, Z., Zhang, J., Wang, J., Zen, K., Xiang, Y., Wang, D., & Zhang, C. Y. (2010). Hypoxia induces PGC-1α expression and mitochondrial biogenesis in the myocardium of TOF patients. Cell Research, 20(6), 676-87. https://doi.org/10.1038/cr.2010.46
Zhu L, et al. Hypoxia Induces PGC-1α Expression and Mitochondrial Biogenesis in the Myocardium of TOF Patients. Cell Res. 2010;20(6):676-87. PubMed PMID: 20368732.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hypoxia induces PGC-1α expression and mitochondrial biogenesis in the myocardium of TOF patients. AU - Zhu,Lingyun, AU - Wang,Qiang, AU - Zhang,Lin, AU - Fang,Zhixiang, AU - Zhao,Fang, AU - Lv,Zhiyuan, AU - Gu,Zuguang, AU - Zhang,Junfeng, AU - Wang,Jin, AU - Zen,Ke, AU - Xiang,Yang, AU - Wang,Dongjin, AU - Zhang,Chen-Yu, Y1 - 2010/04/06/ PY - 2010/4/7/entrez PY - 2010/4/7/pubmed PY - 2011/1/11/medline SP - 676 EP - 87 JF - Cell research JO - Cell Res. VL - 20 IS - 6 N2 - PGC-1alpha, a potent transcriptional coactivator, is the major regulator of mitochondrial biogenesis and activity in the cardiac muscle. The dysregulation of PGC-1alpha and its target genes has been reported to be associated with congenital and acquired heart diseases. By examining myocardium samples from patients with Tetralogy of Fallot, we show here that PGC-1alpha expression levels are markedly increased in patients compared with healthy controls and positively correlated with the severity of cyanosis. Furthermore, hypoxia significantly induced the expression of PGC-1alpha and mitochondrial biogenesis in cultured cardiac myocytes. Mechanistic studies suggest that hypoxia-induced PGC-1alpha expression is regulated through the AMPK signaling pathway. Together, our data indicate that hypoxia can stimulate the expression of PGC-1alpha and mitochondrial biogenesis in the cardiac myocytes, and this process might provide a potential adaptive mechanism for cardiac myocytes to increase ATP output and minimize hypoxic damage to the heart. SN - 1748-7838 UR - https://www.unboundmedicine.com/medline/citation/20368732/Hypoxia_induces_PGC_1α_expression_and_mitochondrial_biogenesis_in_the_myocardium_of_TOF_patients_ L2 - http://dx.doi.org/10.1038/cr.2010.46 DB - PRIME DP - Unbound Medicine ER -