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Editorial Board Members/Copyright 编辑委员会成员/版权

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-12-12 DOI: 10.1016/S1355-8145(24)00137-8

引用次数: 0

Cover and caption 封面及标题

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-12-12 DOI: 10.1016/S1355-8145(24)00136-6

引用次数: 0

Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications 骨关节炎中内质网应激介导的细胞凋亡和自噬：从分子机制到治疗应用。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-11-19 DOI: 10.1016/j.cstres.2024.11.005

Yifan Lu , Jing Zhou , Hong Wang , Hua Gao , Eryu Ning , Zhiqiang Shao , Yuefeng Hao , Xing Yang

{"title":"Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications","authors":"Yifan Lu , Jing Zhou , Hong Wang , Hua Gao , Eryu Ning , Zhiqiang Shao , Yuefeng Hao , Xing Yang","doi":"10.1016/j.cstres.2024.11.005","DOIUrl":"10.1016/j.cstres.2024.11.005","url":null,"abstract":"<div><div>Osteoarthritis (OA) is characterized primarily by the degeneration of articular cartilage, with a high prevalence and disability rate. The functional phenotype of chondrocytes, as the sole cell type within cartilage, is vital for OA progression. Due to the avascular nature of cartilage and its limited regenerative capacity, repair following injury poses significant challenges. Various cellular stressors, including hypoxia, nutrient deprivation, oxidative stress, and collagen mutations, can lead to the accumulation of misfolded proteins in the endoplasmic reticulum (ER), resulting in ER stress (ERS). In response to restore ER homeostasis as well as cellular vitality and function, a series of adaptive mechanisms are triggered, including the unfolded protein response, ER-associated degradation, and ER-phagy. Prolonged or severe ERS may exceed the adaptive capacity of cells, leading to dysregulation in apoptosis and autophagy—key pathogenic factors contributing to chondrocyte damage and OA progression. This review examines the relationship between ERS in OA chondrocytes and both apoptosis and autophagy in order to identify potential therapeutic targets and strategies for prevention and treatment of OA.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 805-830"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of the FKBP51–Hsp90 complex in Alzheimer’s disease: An emerging new drug target FKBP51-Hsp90复合物在阿尔茨海默病中的作用：一个新兴的新药物靶点。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-11-29 DOI: 10.1016/j.cstres.2024.11.006

Xavier Jeanne , Zsolt Török , László Vigh , Chrisostomos Prodromou

{"title":"The role of the FKBP51–Hsp90 complex in Alzheimer’s disease: An emerging new drug target","authors":"Xavier Jeanne , Zsolt Török , László Vigh , Chrisostomos Prodromou","doi":"10.1016/j.cstres.2024.11.006","DOIUrl":"10.1016/j.cstres.2024.11.006","url":null,"abstract":"<div><div>With increasing age comes the inevitable decline in proteostasis, where chaperone and co-chaperone activity becomes imbalanced. These changes lead to global disturbances and pathogenic rewiring of the chaperone system into epichaperones consisting of protein networks that are ultimately dysfunctional. Such imbalances in proteostasis may favor mechanisms that can lead to neurological diseases, such as Alzheimer’s disease (AD). Consequently, there has been an increase in research activity toward finding small molecules that can re-balance the chaperone and co-chaperone machinery to counter the effects of disease resulting from old age. The Hsp90 co-chaperone FKBP51 has recently been identified as a protein whose induction not only increases with age but is elevated further in AD cells. Significantly, FKBP51 plays a role in the Hsp90-dependent isomerization of tau, which in turn influences its phosphorylation and susceptibility to aggregation. We hypothesize that FKBP51 is a major player that is able to elicit tauopathy in response to amyloid-beta senile plaques that damage the brain. We propose that elevated FKBP51 levels result in an abnormal FKBP51–Hsp90 activity that alters the normal processing of tau, which manifests as hyperphosphorylation and oligomerization of tau. Thus, the Hsp90–FKBP51 complex is emerging as a drug target against AD. In support of this idea, the structure of the FKBP51–Hsp90 complex was recently described, and significantly, the small-molecule dihydropyridine LA1011 was shown to be able to disrupt the Hsp90–FKBP51 complex. LA1011 was previously shown to effectively prevent neurodegeneration in the APPxPS1 AD transgenic mouse model. This review looks at the role of Hsp90 and its co-chaperones in AD with a focus on FKBP51.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 792-804"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pyrotinib induces cell death in HER2-positive breast cancer via triggering HSP90-dependent HER2 degradation and ROS/HSF-1-dependent oxidative DNA damage 派罗替尼通过引发依赖HSP90的HER2降解和依赖ROS/HSF-1的氧化性DNA损伤，诱导HER2阳性乳腺癌细胞死亡。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-11-18 DOI: 10.1016/j.cstres.2024.11.004

Xiaomin Gao , Xu Guo , Wenbo Yuan , Sunmin Jiang , Zihong Lu , Qing Luo , Yuan Zha , Ling Wang , Shu Li , Ke Wang , Xue Zhu , Ying Yao

{"title":"Pyrotinib induces cell death in HER2-positive breast cancer via triggering HSP90-dependent HER2 degradation and ROS/HSF-1-dependent oxidative DNA damage","authors":"Xiaomin Gao , Xu Guo , Wenbo Yuan , Sunmin Jiang , Zihong Lu , Qing Luo , Yuan Zha , Ling Wang , Shu Li , Ke Wang , Xue Zhu , Ying Yao","doi":"10.1016/j.cstres.2024.11.004","DOIUrl":"10.1016/j.cstres.2024.11.004","url":null,"abstract":"<div><div>HER2-positive breast cancer (HER2+ BC) is distinguished by its poor prognosis, propensity for early onset, and high risk of recurrence and metastasis. Consequently, anti-HER2-targeted therapy has emerged as a principal strategy in the treatment of this form of breast cancer. Pyrotinib, a novel irreversible pan-HER2 tyrosine kinase inhibitor, has brought fresh hope to patients with advanced HER2+ breast cancer. In this study, we conducted a comprehensive exploration of pyrotinib’s antitumor mechanism. The <em>in vitro</em> results showed that pyrotinib significantly inhibited SKBR3 cells viability and induced apoptosis by promoting HER2 endocytosis and ubiquitylation, leading to HER2 degradation through the displacement of HSP90 from HER2. Beyond targeting the HER2 signaling pathway, pyrotinib also induced DNA damage, which was mediated by the activation of the reactive oxygen species/heat shock factor 1 signaling pathway and the downregulation of proliferating cell nuclear antigen expression. Furthermore, the <em>in vivo</em> results demonstrated a pronounced anticancer effect of pyrotinib in the SKBR3 xenograft mouse model, concomitant with a reduction in HER2 expression. In summary, our findings provide novel insights into the mechanism of pyrotinib in the treatment of HER2+ BC.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 777-791"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “The mechanism and therapeutic strategies in doxorubicin induced cardiotoxicity: Role of programmed cell death” [Cell Stress Chaperones. 2024;29:666-680] 多柔比星诱发心脏毒性的机制和治疗策略：细胞应激合子的作用》[Cell Stress Chaperones.］

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-10-24 DOI: 10.1016/j.cstres.2024.10.005

Yanzhao Li , Jing Yan , Pingzhen Yang

引用次数: 0

The heat shock factor code: Specifying a diversity of transcriptional regulatory programs broadly promoting stress resilience 热休克因子代码：明确转录调控程序的多样性，广泛促进应激恢复能力。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-10-23 DOI: 10.1016/j.cstres.2024.10.006

Milad J. Alasady , Marc L. Mendillo

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Protective role of short-chain fatty acids on intestinal oxidative stress induced by TNF-α 短链脂肪酸对 TNF-α 诱导的肠道氧化应激的保护作用

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1016/j.cstres.2024.11.002

Miguel Ferrer , Berta Buey , Laura Grasa , Jose Emilio Mesonero , Eva Latorre

{"title":"Protective role of short-chain fatty acids on intestinal oxidative stress induced by TNF-α","authors":"Miguel Ferrer , Berta Buey , Laura Grasa , Jose Emilio Mesonero , Eva Latorre","doi":"10.1016/j.cstres.2024.11.002","DOIUrl":"10.1016/j.cstres.2024.11.002","url":null,"abstract":"<div><div>Inflammatory bowel diseases (IBDs) are driven by an exaggerated inflammatory response, which leads to a marked increase in oxidative stress. This, in turn, exacerbates the inflammatory process and causes significant cellular and tissue damage. Intestinal dysbiosis, a common observation in IBD patients, alters the production of bacterial metabolites, including short-chain fatty acids (SCFAs), which are key by-products of dietary fiber fermentation. While the role of SCFAs in intestinal physiology is still being elucidated, this study aimed to investigate their effects on intestinal oxidative stress, particularly under inflammatory conditions induced by the proinflammatory mediator tumor necrosis factor alpha (TNF-α). The Caco-2/TC7 cell line was employed as an in vitro model of the intestinal epithelium, and the cells were treated with a range of SCFAs, including acetate, propionate, and butyrate. The levels of protein and lipid oxidation were quantified, as well as the activity of antioxidant enzymes. Our findings demonstrate that microbiota-derived SCFAs can effectively mitigate TNF-α-induced oxidative stress by modulating antioxidant enzyme activity. The proinflammatory mediator TNF-α induces lipid peroxidation by inhibiting catalase and glutathione peroxidase activities. SCFAs are able to upregulate antioxidant enzyme activity to restore lipid oxidative levels. These results underscore the critical role of the gut microbiota in maintaining intestinal homeostasis and highlight the therapeutic potential of SCFAs in managing oxidative stress-related pathologies.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 769-776"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In memoriam James S. Clegg (1933–2024) 纪念詹姆斯-克莱格（James S. Clegg，1933-2024 年）。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-10-11 DOI: 10.1016/j.cstres.2024.10.003

Lawrence E. Hightower

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Regulation of chondrocyte apoptosis in osteoarthritis by endoplasmic reticulum stress 内质网应激对骨关节炎中软骨细胞凋亡的调节作用

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 Epub Date: 2024-11-06 DOI: 10.1016/j.cstres.2024.11.001

Renzhong Li , Kui Sun

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