Regulation of senescence-associated secretory phenotypes in osteoarthritis by cytosolic UDP-GlcNAc retention and O-GlcNAcylation by Donghyun Kang, Jeeyeon Lee, Geunho Yook, Sehan Jeong, Jungkwon Shin, Mi-Sung Kim, Yi-Jun Kim, Hyeryeon Jung, Jinsung Ahn, Tae Woo Kim, Moon Jong Chang, Chong Bum Chang, Seung-Baik Kang, Won Ho Yang, Yong-ho Lee, Jin Won Cho, Eugene C. Yi, Chanhee Kang, Jin-Hong Kim

“…Mechanistically, upregulated O-GlcNAcylation governs the senescence-associated secretory phenotype (SASP) by stabilizing GATA4 via O-GlcNAcylation at S406, which compromises its degradation by p62-mediated selective autophagy. …”
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Bergapten alleviates senescence of chondrocytes in osteoarthritis by YE Yuanlan, LIU Kaiwen, PAN Yiming

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Plants and fungi metabolites as novel autophagy inducers and senescence inhibitors by Rivka Ofir

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Inhibition of miMOMP-induced SASP to combat age-related disease by Xiaoli Liao, Zhennan Guo, Zhennan Guo, Mouhai He, Yichun Zhang

Subjects: “…SASP (senescence-associated secretory phenotype)…”
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Moving from an “anti-aging” paradigm toward the concept of “disease-free aging”: the role of senolytics in modern medicine by Ivan Aprahamian, Andréia Pain, Virgílio Garcia Moreira

“…Senescent cells increase with aging and are related to the promotion of inflammation and neoplasia through the senescence-associated secretory phenotype (SASP). These cells are closely related to the biological aging process and, most importantly, to age-associated diseases, such as osteoporosis and osteoarthritis. …”
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T-2 toxin induces senescence in human neuroblastoma SH-SY5Y cells by regulating the HIF-1α/p53/p21 pathway by Yating Wang, Xu Wang, Qinghua Wu

“…Notably, HIF-1α regulated the expression of cell cycle inhibitory proteins (p16, p21, p53) and senescence-associated secretory phenotype factors (IL-8, IL-6, CCL2), along with the expression of senescence-associated β-galactosidase, thereby exacerbating T-2 toxin-induced cellular senescence. …”
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The Intersection of Epigenetics and Senolytics in Mechanisms of Aging and Therapeutic Approaches by Daiana Burdusel, Thorsten R. Doeppner, Roxana Surugiu, Dirk M. Hermann, Denissa Greta Olaru, Aurel Popa-Wagner

“…Senolytics, a class of drugs targeting and eliminating senescent cells, address the accumulation of dysfunctional cells that contribute to tissue degradation and chronic inflammation through the senescence-associated secretory phenotype. This scoping review examines the intersection of epigenetic mechanisms and senolytic therapies in aging, focusing on their combined potential for therapeutic interventions. …”
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Increase of circulating IGFBP-4 following genotoxic stress and its implication for senescence by Nicola Alessio, Tiziana Squillaro, Giovanni Di Bernardo, Giovanni Galano, Roberto De Rosa, Mariarosa AB Melone, Gianfranco Peluso, Umberto Galderisi

“…Senescent cells secrete several molecules, collectively named senescence-associated secretory phenotype (SASP). In the SASP of cells that became senescent following several in vitro chemical and physical stress, we identified the IGFBP-4 protein that can be considered a general stress mediator. …”
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The crosstalk between senescence, tumor, and immunity: molecular mechanism and therapeutic opportunities by Zehua Wang, Chen Chen, Jiaoyu Ai, Yaping Gao, Lei Wang, Shurui Xia, Yongxu Jia, Yanru Qin

“…Specifically, senescent cells display a unique senescence‐associated secretory phenotype that releases a diverse array of soluble factors affecting the TME. …”
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Chloride intracellular channel CLIC3 mediates fibroblast cellular senescence by interacting with ERK7 by Changjiao Luan, Yue Gao, Jun Zhao, Xiaohui Zhang, Chaofan Wang, Wentao Sun, Yucheng Li, Xinxing Yang, Jiaxiao Chen, Weili Liu, Weijuan Gong, Xingjie Ma

“…Furthermore, our findings revealed that the knockdown of CLIC3 mitigated intracellular chloride ion lose, mitochondrial dysfunction, nuclear enlargement, DNA damage, CS progression, and expression of senescence-associated secretory phenotype (SASP) triggered by bleomycin. …”
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The role of SASP in ischemic stroke: a deep dive into cellular mechanisms by Dong Xie, Yang Liu, Fang-Biao Xu, Jin-Sheng Zhang

“…Aging, a prominent risk factor, implicates the senescence-associated secretory phenotype (SASP) in IS pathogenesis. …”
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Karyopherin Alpha 2-Expressing Pancreatic Duct Glands and Intra-Islet Ducts in Aged Diabetic C414A-Mutant-CRY1 Transgenic Mice by Satoshi Okano, Akira Yasui, Shin-ichiro Kanno, Kennichi Satoh, Masahiko Igarashi, Osamu Nakajima

“…Our earlier studies demonstrated that cysteine414- (zinc-binding site of mCRY1-) alanine mutant mCRY1 transgenic mice (Tg mice) exhibit diabetes characterized by the reduction of β-cell proliferation and by β-cell dysfunction, presumably caused by senescence-associated secretory phenotype- (SASP-) like characters of islets. …”
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RETRACTED ARTICLE: P16INK4a Deletion Ameliorated Renal Tubulointerstitial Injury in a Stress-induced Premature Senescence Model of Bmi-1 Deficiency by Jianliang Jin, Jianguo Tao, Xin Gu, Zhenzhen Yu, Rong Wang, Guoping Zuo, Qing Li, Xianhui Lv, Dengshun Miao

“…Abstract To determine whether p16INK4a deletion ameliorated renal tubulointerstitial injury by inhibiting a senescence-associated secretory phenotype (SASP) in Bmi-1-deficient (Bmi-1−/−) mice, renal phenotypes were compared among 5-week-old Bmi-1 and p16INK4a double-knockout, and Bmi-1−/− and wild-type mice. …”
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Protective effect of adiponectin on oxidative stress-induced ovarian granulosa cell senescence in geese by Yan Zheng, Yunqiao Qiu, Ming Gao, Qianhui Wang, Lei Yu, Zhongzan Cao, Xinhong Luan

“…The results showed that ADPN could alleviate oxidative stress and cell cycle arrest in GCs, reduce the expression of the senescence-associated secretory phenotype (SASP)-related genes IL-6 and IL-8, regulate the metabolic capacity of GCs, reduce the accumulation of SA-β-gal, maintain telomere length, and alleviate the senescence of GCs induced by D-gal. …”
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Human placental extract improves liver cirrhosis in mice with regulation of macrophages and senescent cells by Natsuki Ishikawa, Yusuke Watanabe, Yuichirou Maeda, Tomoaki Yoshida, Naruhiro Kimura, Hiroyuki Abe, Akira Sakamaki, Hiroteru Kamimura, Takeshi Yokoo, Kenya Kamimura, Atsunori Tsuchiya, Shuji Terai

“…Furthermore, there was a decrease in the number of senescent cells in the liver and the mRNA levels of secrete senescence-associated secretory phenotype factors and Cdkn2a (p16). …”
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Human proximal tubular epithelial cell interleukin-1 receptor signalling triggers G2/M arrest and cellular senescence during hypoxic kidney injury by Kurt T. K. Giuliani, Purba Nag, Benjamin C. Adams, Xiangju Wang, Seokchan Hong, Anca Grivei, Rebecca L. Johnston, Nicola Waddell, Kenneth K. C. Ho, Yilin Tian, Muhammad Ali Khan, Chang Seong Kim, Monica S. Y. Ng, Glenda Gobe, Jacobus P. J. Ungerer, Josephine M. Forbes, Helen G. Healy, Andrew J. Kassianos

“…Hypoxia+IL-1β-treated PTECs displayed signatures of cellular senescence, with reduced proliferation, G2/M cell cycle arrest, increased p21 expression, elevated senescence-associated β-galactosidase (SA-β-gal) activity and increased production of pro-inflammatory/fibrotic senescence-associated secretory phenotype (SASP) factors compared to normoxic conditions. …”
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NEAT1 regulates BMSCs aging through disruption of FGF2 nuclear transport by Zifei Wang, Wenyu Zhen, Qing Wang, Yuqiang Sun, Siyu Jin, Sensen Yu, Xing Wu, Wenhao Zhang, Yulong Zhang, Fei Xu, Rui Wang, Yuxuan Xie, Wansu Sun, Jianguang Xu, Hengguo Zhang

“…Within NEAT1 knockdown, hallmarks of cellular aging, including senescence-associated secretory phenotype (SASP), p16, and p21, were significantly downregulated. …”
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Novel Approach to Bile Duct Damage in Primary Biliary Cirrhosis: Participation of Cellular Senescence and Autophagy by Motoko Sasaki, Yasuni Nakanuma

“…Furthermore, senescent BECs may modulate the microenvironment around bile ducts by expressing various chemokines and cytokines called senescence-associated secretory phenotypes and contribute to the pathogenesis in PBC.…”
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lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases by Lulingxiao Nie, Peng Zhang, Qian Wang, Xinyi Zhou, Qi Wang

“…Autophagy defects, oxidative stresses, senescence-associated secretory phenotypes (SASPs), and DNA damage generally contribute to inflammaging and are largely regulated by numerous lncRNA through two-level vicious cycles disrupting cellular homeostasis: (1) inflammaging and the cellular senescence cascade and (2) autophagy defects, oxidative stress, and the SASP cascade. …”
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The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies by Liu S, Zhang G, Li N, Wang Z, Lu L

“…Age-related cellular and immune dysfunctions, including cellular senescence, senescence-associated secretory phenotypes (SASPs), and immunosenescence, significantly contribute to joint degeneration. …”
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