Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis.

By J. J. Lehman, P. Barger, A. Kovács, J. Saffitz, D. Medeiros, D. Kelly. Journal of Clinical Investigation, 2000

1,337 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c0027827251d0011a63258f83dd10c7c58938654

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Citations in the corpus

Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “As we have seen, gain-of-function experiments have established that overexpression of either PGC-1 or PGC-1 can orchestrate massive increases in mitochondrial biogenesis both in cultured cells and in mouse tissues (10, 116, 236).”
The mitophagy pathway and its implications in human diseases (2023, background): “PGC-1α overexpression significantly promotes content of mtDNA and mitochondrial in myocytes of transgenic mice.(163,164) PGC-1α is now recognized as a master regulator of mitochondrial biogenesis, coordinating essential proteins expression for mitochondrial biogenesis via transcription factors NRF1/”
mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation. (2013, background): “Consistently, the assessment of mitochondrial functions upon ectopic expression of the transcriptional coactivators (e.g., PGC-1a) has typically been performed after 48 hr or longer (Lehman et al., 2000; St-Pierre et al., 2003).”
Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres (2002, background): “PGC-1α is expressed in skeletal muscle, and powerfully induces mitochondrial biogenesis when expressed ectopically in skeletal and cardiac myocyte”
Regulation of Muscle Fiber Type and Running Endurance by PPARδ (2004, background): “These effects appear to be direct consequences of PPAR d activation, as levels of PGC-1 a , a coactivator involved in muscle ﬁber switch and mitochondrial biogenesis (Wu et al. 1999; Lehman et al. 2000; Lin et al. 2002), remained unchanged.”
Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF (2013, positive): “PGC1a drives mitochondrial biogenesis in multiple contexts, including brown and white adipocytes (Wu et al., 1999; Uldry et al., 2006), skeletal muscle (Lin et al., 2002), and the heart (Lehman et al., 2000).”
Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “PGC-1α is induced at birth in the mouse heart when there is a striking increase in mitochondrial biogenesis.(121,122) Studies have found that fasting is associated with both increased mitophagy(123) and rapid upregulation of PGC-1α in heart tissues.”
Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. (2006, background): “PGC-1a has emerged as a master regulator of mitochondrial biogenesis and respiration (Kelly and Scarpulla, 2004; Lehman et al., 2000; Lin et al., 2002; Puigserver et al., 1998; Wu et al., 1999).”
Mitochondrial Energetics in the Heart in Obesity-Related Diabetes (2007, background): “Support for this comes from studies in which forced overexpression of PGC-1 in the heart leads to mitochondrial biogenesis that is maladaptive (39,40).”