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Multiplexed single-cell imaging reveals diverging subpopulations with distinct senescence phenotypes during long-term senescence induction.
Geroscience
January 2025
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Cellular senescence is a phenotypic state that contributes to the progression of age-related disease through secretion of pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Understanding the process by which healthy cells become senescent and develop SASP factors is critical for improving the identification of senescent cells and, ultimately, understanding tissue dysfunction. Here, we reveal how the duration of cellular stress modulates the SASP in distinct subpopulations of senescent cells.
View Article and Find Full Text PDFDifferent expression of circulating microRNA profile in tibetan OSAHS with metabolic syndrome patients.
Sci Rep
January 2025
Department of Respiratory medicine, Taian 88 Hospital, Taian, 271000, People's Republic of China.
Recent empirical investigations reinforce the understanding of a profound interconnection between metabolic functions and Obstructive Sleep Apnea-hypopnea Syndrome (OSAHS). This study identifies distinctive miRNA signatures in OSAHS with Metabolic Syndrome (Mets) patients from healthy subjects, that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. In this study, OSAHS with MetS patients showed significantly higher Apnea Hyponea Index(AHI), but lower oxygen desaturation index(ODI 4/h) and minimum pulse oxygen saturation(SpO).
View Article and Find Full Text PDFACOX1 activates autophagy via the ROS/mTOR pathway to suppress proliferation and migration of colorectal cancer.
Sci Rep
January 2025
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, Jiangsu, China.
Acyl-CoA oxidase 1 (ACOX1), a member of the acyl-coenzyme A oxidase family, is considered a crucial regulator whose dysregulation is implicated in the occurrence and progression of various cancers. This study aims to elucidate the impact of ACOX1 in CRC, shedding light on its potential as a therapeutic target. Through analysis of the GEO dataset, it was found that ACOX1 is significantly downregulated in colorectal cancer (CRC), and this lower expression level is associated with a worse prognosis.
View Article and Find Full Text PDFLINC00626 drives tamoxifen resistance in breast cancer cells by interaction with UPF1.
Sci Rep
January 2025
The Second Department of Critical Care Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China.
Although tamoxifen is commonly utilized as adjuvant therapy for Estrogen Receptor alpha (ERα)-positive breast cancer patients, approximately 30-50% of individuals treated with tamoxifen experience relapse. Therefore, it is essential to investigate additional factors besides ERα that influence the estrogen response. In this study, cross-analysis of databases were performed, and the results revealed a significant association between LINC00626 and ERα signaling as well as increased expression levels of this gene in tamoxifen-resistant cells.
View Article and Find Full Text PDFWhen two signals cross paths: cGAS-STING and ER stress in kidney disease progression.
Kidney Int
February 2025
Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan. Electronic address:
Previous reports have suggested that both the endoplasmic reticulum (ER) stress and cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathways contribute to the progression of chronic kidney disease; however, the relationship between these 2 pathways in kidney injury has not been fully elucidated. Andrade-Silva et al. revealed that the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway can enhance ER stress through the protein kinase R-like ER kinase (PERK)-mediated signaling cascade in kidney tubular epithelial cells and sequentially augment fibrosis during kidney injury.
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