. 2021 Apr 28;22(9):4670. doi: 10.3390/ijms22094670

Table 1.

PGC1α activity on bone metabolism in vitro and in vivo.

PGC1α Activity on Bone Metabolism
Increases Osteocalcin expression together with Nuclear related receptor-1 [8] Enhances Osteocalcin promoter activity interacting with Estrogen-related receptor alpha [9] Restores the inhibition of osteogenic differentiation and mitochondrial activity Sirtuin 3 knockdown-induced [10] Upregulates many key factors involved in osteoblast and osteocyte differentiation [11]	PGC1α deletion causes a reduction in cortical thickness and in osteocalcin and collagen type I α 1 levels [12] PGC1α/β deficiency results in cortical and trabecular parameter reduction [11] PGC1α absence induces marrow adipose tissue accumulation [13] PGC1α activation in leptin receptor-deficient diabetic mice increases osteoblastic gene expression and inhibits atrogene transcription [14]

PGC1α Activity on Bone Metabolism

In Vitro

In Vivo

Increases Osteocalcin expression together with Nuclear related receptor-1 [8]
Enhances Osteocalcin promoter activity interacting with Estrogen-related receptor alpha [9]
Restores the inhibition of osteogenic differentiation and mitochondrial activity Sirtuin 3 knockdown-induced [10]
Upregulates many key factors involved in osteoblast and osteocyte differentiation [11]

PGC1α deletion causes a reduction in cortical thickness and in osteocalcin and collagen type I α 1 levels [12]
PGC1α/β deficiency results in cortical and trabecular parameter reduction [11]
PGC1α absence induces marrow adipose tissue accumulation [13]
PGC1α activation in leptin receptor-deficient diabetic mice increases osteoblastic gene expression and inhibits atrogene transcription [14]