Results 121 to 130 of about 8,472,936 (269)

Genetic Ablation and Multi‐Omics Profiling Reveal CEP55 as a Key Driver of Tumorigenesis in Diverse Cancer Models

open access: yesAdvanced Science, EarlyView.
Genetic ablation of Cep55 in Pten‐deficient mouse models delays tumorigenesis. Integrated multi‐omics analyses (proteomics, phosphoproteomics, and spatial transcriptomics) reveal that CEP55 regulates oncogenic signaling (RAS/ERK, PI3K/AKT), integrin/FAK‐mediated adhesion, extracellular matrix (ECM) remodeling, and endocytosis.
Behnam Rashidieh   +22 more
wiley   +1 more source

The role of the senescence-associated secretory phenotype in cardiovascular disease among the elderly

open access: yesEuropean Journal of Internal Medicine
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in the elderly, driven not only by traditional risk factors but also by biological aging processes such as cellular senescence. Senescent cells accumulate in cardiovascular tissues with age and secrete a complex mix of pro-inflammatory cytokines, chemokines, proteases ...
Henry Sutanto   +3 more
openaire   +2 more sources

Epilipidomics of Senescent Dermal Fibroblasts Identify Lysophosphatidylcholines as Pleiotropic Senescence-Associated Secretory Phenotype (SASP) Factors

open access: yes, 2020
Während des Alterns sammelt die Haut seneszente Zellen an. Die vorübergehende Anwesenheit von seneszenten Zellen, gefolgt von ihrer Clearance durch das Immunsystem, ist wichtig für die Gewebereparatur und Homöostase.
Pils, Vera; orcid:   +26 more
core   +1 more source

YAP1‐Driven Pathogenic Fibro‐Adipogenic Progenitors Secrete IL‐6 and FGF21 to Mediate Muscle‐Bone Crosstalk and Promote Bone Loss

open access: yesAdvanced Science, EarlyView.
Fibro‐adipogenic progenitors (FAPs) in atrophic muscle undergo YAP1‐driven pathogenic activation, secreting IL‐6 and FGF21 as bone‐catabolic myokines that mediate muscle‐bone crosstalk and promote bone loss. Genetic or pharmacological targeting of this YAP1‐FAP‐myokine axis rescues skeletal deterioration, identifying FAP‐derived myokines as therapeutic
Xiaoyu Cai   +16 more
wiley   +1 more source

HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci [PDF]

open access: yes, 2016
Cellular senescence is a stable cell growth arrest that is characterized by the silencing of proliferation-promoting genes through compaction of chromosomes into senescence-associated heterochromatin foci (SAHF).
Bitler B.   +11 more
core  

USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis

open access: yesAdvanced Science, EarlyView.
This study reveals that USP5 drives vascular smooth muscle cell senescence and atherosclerosis by stabilizing TGFBR1, suppressing IDH2, and promoting glycolytic reprogramming, identifying the USP5‐TGFBR1‐IDH2 axis as a potential therapeutic target. ABSTRACT Vascular smooth muscle cell (VSMC) senescence contributes importantly to atherosclerotic plaque ...
Xinhai Cui   +5 more
wiley   +1 more source

Cellular senescence of renal tubular epithelial cells in acute kidney injury

open access: yesCell Death Discovery
Cellular senescence represents an irreversible state of cell-cycle arrest during which cells secrete senescence-associated secretory phenotypes, including inflammatory factors and chemokines.
Juan Chen   +7 more
doaj   +1 more source

Fibrillarin Resists Cellular Senescence Via SIRT1‐Dependent Nicotinamide Metabolism and Its Inhibition Sensitizes Senolytic Therapy in Esophageal Squamous Cell Carcinoma

open access: yesAdvanced Science, EarlyView.
FBL directly binds to and stabilizes SIRT1 by blocking its ubiquitin‐proteasome degradation, thereby sustaining nicotinamide metabolism and redox homeostasis to counteract cellular senescence in ESCC. Genetic and pharmacological suppression of FBL sensitizes tumor cells to senolytic therapy.
Xing Jin   +9 more
wiley   +1 more source

Maternal Exercise Rescues Embryonic Osteogenesis Impaired due to POLG Mutation Through a Potential Apelin‐ATF4 Axis

open access: yesAdvanced Science, EarlyView.
Maternal exercise (ME) increases apelin abundance across maternal and fetal tissues and is associated with improved fetal osteogenesis under POLG mutation‐induced mitochondrial dysfunction. Apelin‐APJ signaling is linked to enhanced mitochondrial function, Akt phosphorylation, and ATF4‐RUNX2 association, supporting coordinated fetal bone remodeling ...
Song Ah Chae   +5 more
wiley   +1 more source

OTUD6A‐Mediated Deubiquitination of PRDX1 Protects Against Oral Ulcer by Restoring Mitochondrial Function

open access: yesAdvanced Science, EarlyView.
In human oral keratinocytes, OTUD6A promoted cell migration by deubiquitinating and stabilizing PRDX1. Conversely, OTUD6A deficiency reduced PRDX1 stability, triggering mitochondrial dysfunction and aggravating OU progression. ABSTRACT Oral ulcers (OU), as the most highly prevalent and recurrent oral mucosal lesion, have an unclear pathogenesis that ...
Xiaoyu Sun   +15 more
wiley   +1 more source

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