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AMPK signaling in energy control, cartilage biology, and osteoarthritis

Citation

Yi, D and Yu, H and Lu, K and Ruan, C and Ding, C and Tong, L and Zhao, X and Chen, D, AMPK signaling in energy control, cartilage biology, and osteoarthritis, Frontiers in Cell and Developmental Biology, 9 pp. 1-14. ISSN 2296-634X (2021) [Refereed Article]


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Copyright Statement

Copyright 2021 Yi, Yu, Lu, Ruan, Ding, Tong, Zhao and Chen. This is an openaccess article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

DOI: doi:10.3389/fcell.2021.696602

Abstract

The adenosine monophosphate (AMP)-activated protein kinase (AMPK) was initially identified as an enzyme acting as an "energy sensor" in maintaining energy homeostasis via serine/threonine phosphorylation when low cellular adenosine triphosphate (ATP) level was sensed. AMPK participates in catabolic and anabolic processes at the molecular and cellular levels and is involved in appetite-regulating circuit in the hypothalamus. AMPK signaling also modulates energy metabolism in organs such as adipose tissue, brain, muscle, and heart, which are highly dependent on energy consumption via adjusting the AMP/ADP:ATP ratio. In clinics, biguanides and thiazolidinediones are prescribed to patients with metabolic disorders through activating AMPK signaling and inhibiting complex I in the mitochondria, leading to a reduction in mitochondrial respiration and elevated ATP production. The role of AMPK in mediating skeletal development and related diseases remains obscure. In this review, in addition to discuss the emerging advances of AMPK studies in energy control, we will also illustrate current discoveries of AMPK in chondrocyte homeostasis, osteoarthritis (OA) development, and the signaling interaction of AMPK with other pathways, such as mTOR (mechanistic target of rapamycin), Wnt, and NF-κB (nuclear factor κB) under OA condition.

Item Details

Item Type:Refereed Article
Keywords:AMPK, chondrocyte, energy balance, osteoarthritis, signaling interaction
Research Division:Biomedical and Clinical Sciences
Research Group:Clinical sciences
Research Field:Rheumatology and arthritis
Objective Division:Health
Objective Group:Clinical health
Objective Field:Diagnosis of human diseases and conditions
UTAS Author:Ding, C (Professor Chang-Hai Ding)
ID Code:146984
Year Published:2021
Web of Science® Times Cited:2
Deposited By:Menzies Institute for Medical Research
Deposited On:2021-10-07
Last Modified:2021-11-24
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