{'fraction_non_alphanumeric': 0.03125, 'fraction_numerical': 0.009259259259259259, 'mean_word_length': 6.587719298245614, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Mitochondrial Biogenesis Is Impaired in Osteoarthritis Chondrocytes but Reversible via 
Peroxisome Proliferator–Activated Receptor γ Coactivator 1α

The etiology of chondrocyte mitochondrial dysfunction in osteoarthritis (OA) is not completely understood. OA chondrocytes are deficient in the metabolic biosensors active AMP‐activated protein kinase (AMPK) and sirtuin 1 (SIRT‐1), which modulate the mitochondrial biogenesis “master regulator” peroxisome proliferator–activated receptor γ coactivator 1α (PGC‐1α). Moreover, PGC‐1α critically mediates AMPK anticatabolic activity in chondrocytes. The aim of this study was to test the hypothesis that mitochondrial biogenesis is deficient in human OA chondrocytes and that this deficiency functionally increases chondrocyte procatabolic responses, which are reversed by activation of the AMPK/SIRT‐1/PGC‐1α pathway.