An important aspect of mitochondria maintenance includes biogenesis to replenish damaged and degraded mitochondrial structures. The regulation of mitochondrial biogenesis is very complex and numerous genes regulate and synchronize protein synthesis from the mitochondrial and nuclear genome. The factors governing these processes include nuclear respiratory factors (NRF1 and NRF2) as well as the nuclear receptors such as peroxisome proliferator receptors (PPARs) and estrogen related receptors (ERRs). Peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1 alpha) binds to NRF1 and NRF2, as well as the nuclear receptors PPAR and ERR, to induce expression of their target genes.
IHC analysis of PGC-1 alpha in mouse prostate
Increased PGC-1 alpha activity results in increased mitochondrial mass and overall mitochondrial function, so PGC-1 alpha is considered to be the master regulator of mitochondrial biogenesis (1). PGC-1 alpha activity is regulated on both expression and post-translational levels, PPARs are a group of ligand-modulated transcription factors that regulate gene-expression programs of metabolic pathways. Endogenous ligands include fatty acids and eicosanoids and thereby allowing the PPARs to link dietary input as well as alterations in cellular metabolism to changes in target gene transcription through PGC-1 alpha activation, and metabolic changes to mitochondrial function (2). PGC-1 alpha activation and the resulting increased mitochondrial biogenesis offer a therapeutic intervention for mitochondrial myopathies and is an open area of research.
1. PMID: 18391175
2. PMID: 17275789
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