Senescent cells secrete bioreactive molecules that promote disease, fibrosis, and aging, yet the molecular mechanisms driving the production of these secreted factors remain incompletely understood. In this issue, Papismadov et al (2024) report that p21 (CDKN1A), known to activate the senescence growth arrest, also regulates expression of extracellular matrix components that promote fibrosis, thereby revealing new therapeutic inroads to target fibrosis and age-related pathologies.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574165 | PMC |
| http://dx.doi.org/10.1038/s44318-024-00245-8 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dose-dependent effects of Nrf2 on the epidermis in chronic skin inflammation.
Dis Model Mech
January 2025
Institute of Molecular Health Sciences, Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.
Atopic dermatitis (AD) is a chronic inflammatory skin disease, characterized by an impaired epidermal barrier and immunological alterations. The activity of the cytoprotective NRF2 transcription factor is reduced in the epidermis of AD patients. To determine the functional relevance of this deficiency, we used mice lacking fibroblast growth factor receptors 1 and 2 in keratinocytes (K5-R1/R2 mice), which exhibit several AD-like symptoms.
View Article and Find Full Text PDFInsights into Structure and Function of Growth Arrest Specific 2 (GAS2).
J Cancer
January 2025
Cyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, China.
Growth arrest specific 2 (GAS2) is a microfilament-associated protein, which is widely distributed in human tissues. It exerts a pivotal influence on various cellular processes, including cytoskeletal regulation, cell cycle progression, apoptosis, and senescence. GAS2 has a dual function in cancer cell growth: on the one hand, it enhances the sensitivity of cancer cells to chemoradiotherapy and prevents malignant transformation of normal cells; but on the other hand, it maintains the growth of cancer cells.
View Article and Find Full Text PDFPersistence and/or Senescence: Not So Lasting at Last?
Cancer Res
January 2025
Medical Department of Hematology, Oncology and Tumor Immunology, Molekulares Krebsforschungszentrum - MKFZ, Campus Virchow Klinikum, Charité - Universitätsmedizin, Berlin, Germany.
Therapy-exposed surviving cancer cells may have encountered profound epigenetic remodeling that renders these drug-tolerant persisters candidate drivers of particularly aggressive relapses. Typically presenting as slow-to-nongrowing cells, persisters are senescent or senescence-like cells. In this issue of Cancer Research, Ramponi and colleagues study mTOR/PI3K inhibitor-induced embryonic diapause-like arrest (DLA) as a model of persistence in lung cancer and melanoma cells and compare this persister condition with therapy-induced senescence in the same cells.
View Article and Find Full Text PDFFBP1 controls liver cancer evolution from senescent MASH hepatocytes.
Nature
January 2025
Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA, USA.
Hepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH). While increasing HCC risk, MASH triggers p53-dependent hepatocyte senescence, which we found to parallel hypernutrition-induced DNA breaks. How this tumour-suppressive response is bypassed to license oncogenic mutagenesis and enable HCC evolution was previously unclear.
View Article and Find Full Text PDF[Mitochondrial transfer contributes to the odontogenic differentiation of dental mesenchymal stem cells].
Zhonghua Kou Qiang Yi Xue Za Zhi
January 2025
Department of Implantology, Stomatological Hospital and Dental School, Tongji University & Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology, Shanghai200072, China.
Article Synopsis
- The study aimed to explore mitochondrial transfer in dental mesenchymal stem cells (MSCs) and its impact on their ability to differentiate into odontogenic cells.
- Flow cytometry, immunostaining, and advanced imaging techniques were utilized to analyze the presence and significance of mitochondrial transfer in these cells, revealing its role in promoting odontogenic differentiation.
- The research found evidence of mitochondrial transfer through structures called tunneling nanotubes (TNTs) and showed that inhibiting this transfer affected key differentiation markers and gene expression related to odontogenesis.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!