Chen Kuang, Taiyang Liao, Lishi Jie, Yibao Wei, Deren Liu, Enrui Hu, Liang Ding, Peimin Wang
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引用次数: 0
Abstract
Osteoarthritis (OA) is a common degenerative joint disease characterized by cartilage destruction and inflammation. This study reveals that activating transcription factor 4 (ATF4) is upregulated in IL-1β-treated chondrocytes and promotes ferroptosis, a form of programmed cell death. Knockdown of ATF4 alleviated cartilage damage and reduced ferroptosis in both cell and mouse models. Mechanistically, ATF4 directly binds to the promoter of nuclear protein 1 (NUPR1) and activates its transcription. Overexpression of NUPR1 reversed the protective effects of ATF4 knockdown, confirming the critical role of the ATF4-NUPR1 axis in mediating ferroptosis and OA progression. These findings identify ATF4 as a key driver of OA via ferroptosis regulation and suggest that targeting the ATF4-NUPR1 pathway may offer a promising therapeutic strategy.
期刊介绍：
The Journal of Physiological Sciences publishes peer-reviewed original papers, reviews, short communications, technical notes, and letters to the editor, based on the principles and theories of modern physiology and addressed to the international scientific community. All fields of physiology are covered, encompassing molecular, cellular and systems physiology. The emphasis is on human and vertebrate physiology, but comparative papers are also considered. The process of obtaining results must be ethically sound.
Fields covered:
Adaptation and environment
Autonomic nervous function
Biophysics
Cell sensors and signaling
Central nervous system and brain sciences
Endocrinology and metabolism
Excitable membranes and neural cell physiology
Exercise physiology
Gastrointestinal and kidney physiology
Heart and circulatory physiology
Molecular and cellular physiology
Muscle physiology
Physiome/systems biology
Respiration physiology
Senses.
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