17β-estradiol attenuates rat articular chondrocyte injury by targeting ASIC1a-mediated apoptosis

Song, Sujing; Tao, Jingjing; Li, Shufang; Qian, Xuewen; Niu, Ruowen; Zhang, Yihao; Chen, Yong; Wang, Ke; Zhu, Faming; Zhu, Chuan‐Jun; Ma, Ganggang; Yangyang,; Peng, Xiaoqing; Zhou, Ren‐Peng; Chen, Feihu

doi:10.1016/j.mce.2020.110742

Cited by 19 publications

(14 citation statements)

References 48 publications

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“…After direct administration of 17β‐estradiol in OCPs and OVX mice, the results showed that 17β‐estradiol enhanced the autophagic response of OCPs and inhibited the antiosteoclastogenic effect of OCPs (Cheng et al, 2020). For chondrocytes, 17β‐estradiol was shown to reduce protein levels of acid‐sensing ion channel 1a (ASIC1a) through the ERα receptor and to induce ASIC1a protein degradation through the autophagy‐lysosomal pathway, which can protect chondrocytes from acid‐induced apoptosis (Song et al, 2020). These results show that the use of estradiol to improve the autophagy ability in cells may be a novel strategy for the treatment of osteoporosis and RA.…”

Section: Therapeutic Potential Of Autophagy In Bone Diseasementioning

confidence: 99%

The role of autophagy in bone homeostasis

Guo

Yang

et al. 2021

Journal Cellular Physiology

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Autophagy is an evolutionarily conserved intracellular process and is considered one of the main catabolism pathways. In the process of autophagy, cells are digested nonselectively or selectively to recover nutrients and energy, so it is regarded as an antiaging process. In addition to the essential role of autophagy in cellular homeostasis, autophagy is a stress response mechanism for cell survival. Here, we review recent literature describing the pathway of autophagy and its role in different bone cell types, including osteoblasts, osteoclasts, and osteocytes. Also discussed is the mechanism of autophagy in bone diseases associated with bone homeostasis, including osteoporosis and Paget's disease. Finally, we discuss the application of autophagy regulators in bone diseases. This review aims to introduce autophagy, summarize the understanding of its relevance in bone physiology, and discuss its role and therapeutic potential in the pathogenesis of bone diseases such as osteoporosis.

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Section: Therapeutic Potential Of Autophagy In Bone Diseasementioning

confidence: 99%

The role of autophagy in bone homeostasis

Guo

Yang

et al. 2021

Journal Cellular Physiology

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“…Moreover, the effect was similar to that observed when PcTx1 was administered alone, suggesting that inhibiting ASIC1a is likely to involve β-estradiol-mediated protection. Furthermore, β-estradiol was able to downregulate the expression of ASIC1a protein through estrogen receptor α (ERα) and protect the chondrocytes from acid-induced damage and apoptosis (Song et al, 2020). Further studies indicate that downregulation of ASIC1a protein expression can be attributed to β-estradiol, which promotes the degradation of ASIC1a protein through the autophagy-lysosomal pathway (Song et al, 2020).…”

Section: Hormonesmentioning

confidence: 99%

“…Furthermore, β-estradiol was able to downregulate the expression of ASIC1a protein through estrogen receptor α (ERα) and protect the chondrocytes from acid-induced damage and apoptosis (Song et al, 2020). Further studies indicate that downregulation of ASIC1a protein expression can be attributed to β-estradiol, which promotes the degradation of ASIC1a protein through the autophagy-lysosomal pathway (Song et al, 2020). These findings suggest that β-estradiol has the potential to be developed as a novel strategy for the treatment of RA by downregulating ASIC1a protein expression.…”

Section: Hormonesmentioning

confidence: 99%

Factors and Molecular Mechanisms Influencing the Protein Synthesis, Degradation and Membrane Trafficking of ASIC1a

Chen

2020

Front. Cell Dev. Biol.

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Acid-sensing ion channels (ASICs) are members of the degenerin/epithelial sodium channel superfamily. They are extracellular pH sensors that are activated by protons. Among all ASICs, ASIC1a is one of the most intensively studied isoforms because of its unique ability to be permeable to Ca 2+. In addition, it is considered to contribute to various pathophysiological conditions. As a membrane proton receptor, the number of ASIC1a present on the cell surface determines its physiological and pathological functions, and this number partially depends on protein synthesis, degradation, and membrane trafficking processes. Recently, several studies have shown that various factors affect these processes. Therefore, this review elucidated the major factors and underlying molecular mechanisms affecting ASIC1a protein expression and membrane trafficking.

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“…In our previous studies, whole-cell patch clamp and intracellular calcium imaging showed that both ASIC current and acid-induced [Ca 2+ ] i increase was attenuated by β-estradiol (Zhou, Leng, Yang, Chen, Hu & Xiong, 2019), suggesting a β-estradiol mediated neuroprotective effect through inhibition of ASIC1a. In recent study, it was found that β-estradiol pretreatment to reduce acid-induced damage and to inhibit cellular apoptosis (Hang et al, 2021;Islander, Jochems, Lagerquist, Forsblad-d'Elia & Carlsten, 2011), subsequent studies have confirmed that this action may be mediated through the autophagy pathway (Song et al, 2020). The observed regulatory effects of estrogen on ASIC1a contribute to a better understanding of the importance of sex with regard to disease manifestations.…”

Section: Secreted Proteins and Peptidesmentioning

confidence: 91%

ASIC1a channel in Age-Related Diseases: Therapeutic Implications

Zhou

Liang

et al. 2022

Preprint

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Age-related diseases have become more common with the advancing age of the worldwide population. Such diseases involve multiple organs, with tissue degeneration and cellular apoptosis. To date, there is a general lack of effective drugs for treatment of most age-related diseases and there is therefore an urgent need to identify novel drug targets for improved treatment. Acid-sensing ion channel 1a (ASIC1a) is a degenerin/epithelial sodium channel family member, which is activated in an acidic environment to regulate pathophysiological processes such as acidosis, inflammation, hypoxia, and ischemia. A large body of evidence suggests that ASIC1a plays an important role in the development of age-related diseases (e.g., stroke, rheumatoid arthritis, Huntington’s disease, and Parkinson’s disease.). Herein we present: 1) a review of ASIC1a channel properties, distribution, and physiological function; 2) a summary of the pharmacological properties of ASIC1a; 3) and a consideration of ASIC1a as a potential therapeutic target for treatment of age-related disease.

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17β-estradiol attenuates rat articular chondrocyte injury by targeting ASIC1a-mediated apoptosis

Cited by 19 publications

References 48 publications

The role of autophagy in bone homeostasis

The role of autophagy in bone homeostasis

Factors and Molecular Mechanisms Influencing the Protein Synthesis, Degradation and Membrane Trafficking of ASIC1a

ASIC1a channel in Age-Related Diseases: Therapeutic Implications

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