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Correction to: Ambient ultraviolet‑B exposure brings quantum changes in phenotypic and molecular signatures of the embryo of a high‑altitude fish, Tor putitora.
Environ Sci Pollut Res Int
January 2025
ICAR-Directorate of Coldwater Fisheries Research, Anusandhan Bhawan, Bhimtal, 263136, Uttarakhand, India.
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 PDFCellular senescence in the tumor with a bone niche microenvironment: friend or foe?
Clin Exp Med
January 2025
Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Cellular senescence is understood to be a biological process that is defined as irreversible growth arrest and was originally recognized as a tumor-suppressive mechanism that prevents further propagation of damaged cells. More recently, cellular senescence has been shown to have a dual role in prevention and tumor promotion. Senescent cells carry a senescence-associated secretory phenotype (SASP), which is altered by secretory factors including pro-inflammatory cytokines, chemokines, and other proteases, leading to the alteration of the tissue microenvironment.
View Article and Find Full Text PDFPhenotypic Heterogeneity of ADTKD-MUC1 Diagnosed Using VNtyper, a Novel Genetic Technique.
Am J Kidney Dis
January 2025
Hereditary Kidney Diseases Laboratory, Inserm UMR 1163, Imagine Institute, Paris Cité University, Paris, France; Department of Genomic Medicine for Rare Diseases, Necker-Enfants Malades Hospital, Assistance publique, Hôpitaux de Paris (AP-HP), Paris, France. Electronic address:
Rationale & Objective: Molecular diagnosis of autosomal dominant tubulointerstitial kidney disease (ADTKD) due to variants in the MUC1 gene has long been challenging since variants lie in a large Variable Number of Tandem Repeat (VNTR) region, making identification impossible using standard short read techniques. Previously, we addressed this diagnostic limitation by developing a computational pipeline, named VNtyper, for easier reliable detection of MUC1 VNTR pathogenic variants from short read sequences. This led to unexpected diagnoses of ADTKD-MUC1 among patients with kidney disease referred for genetic testing, which we report here.
View Article and Find Full Text PDFBlood circulating LncRNAs: SNHG5 and ZFAS1 as biomarkers reflecting cachexia incidence in chronic heart failure patients.
J Nutr
January 2025
Department of Human Physiology of the Chair of Preclinical Sciences, Medical University in Lublin, Lublin, Poland.
Background: Systemic inflammation plays a crucial role in the development and progression of chronic heart failure (CHF) across all phenotypes. The continuous release of pro-inflammatory cytokines causes muscle atrophy and adipocyte breakdown, ultimately resulting in cachexia. Long non-coding RNAs (lncRNAs) are emerging as potential biomarkers associated with cachexia, as they indirectly regulate muscle and fat tissue metabolism.
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