PGC-1α provides a direct link between external physiological stimuli and the regulation of mitochondrial biogenesis, and is a major factor causing slow-twitch rather than fast-twitch muscle fiber types.

[14] PGC-1α protein may also be involved in controlling blood pressure, regulating cellular cholesterol homeostasis, and the development of obesity.

PGC-1α has also been shown to drive NAD biosynthesis to play a large role in renal protection in acute kidney injury.

[28] Moreover, brain-specific isoforms of PGC-1alpha have recently been identified which are likely to play a role in other neurodegenerative disorders such as Huntington's disease and amyotrophic lateral sclerosis.

[35] An independent study confirmed the effect of PGC-1 on polarisation of macrophages towards M2 via STAT6/PPAR gamma and furthermore demonstrated that PGC-1 inhibits proinflammatory cytokine production.

In the metabolic disorder of combined malonic and methylmalonic aciduria (CMAMMA) due to ACSF3 deficiency, there is a massively increased expression of PGC-1α, which is consistent with upregulated beta oxidation.

[citation needed] This article incorporates text from the United States National Library of Medicine, which is in the public domain.