ReviewBiogerontology2024
Aging, ROS, and cellular senescence: a trilogy in the progression of liver fibrosis.
Review in Biogerontology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed.
- Erigeron breviscapus alleviates senescence via AMPK-SIRT1 signaling by modulating FOXO3a-mediated antioxidant defense and p53-dependent apoptosis.Biogerontology · 2026Article
- Integrated Scaffold Redesign and iPSC-Based Screening Reveal Potent Antifibrotic Artemisinin Analogs in Systemic Sclerosis Models.ACS central science · 2026Article
- Pharmacological Potential of Selenoproteins in the Regulation of Oxidative Stress in Liver Diseases.Pharmaceutics · 2026Review
- Review
- Cellular senescence: the "hidden driver" in chronic inflammatory skin disorders.Immunity & ageing : I & A · 2026Review
- Combatting pulmonary fibrosis withChinese herbal medicines · 2026Review
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- The PARP inhibitor olaparib promotes senescence in murine macrophages.GeroScience · 2026Article
- Multimodal computational approaches coupled with experimental assays to identify flavonoids as potent inhibitors of diabetes and AGEs.Journal of computer-aided molecular design · 2026Article
- Bioactive Nanocomposite-Mediated Macrophage Metabolic Shift Orchestrates Pro-Regenerative Healing in the Diabetic Wound Microenvironment.International journal of nanomedicine · 2026Article
- Dual-input dual-compartmental uptake and efflux model based on Gd-EOB-DTPA-enhanced MRI for simultaneously assessing liver function and fibrosis.Translational gastroenterology and hepatology · 2026Article
- Spatial immune niche remodeling of the neutrophil-macrophage axis inchronic liver disease.Frontiers in cell and developmental biology · 2026Review
- Aging Mediates Inflammatory Transformation of Kidney-Resident Macrophages via Thrombospondin-1 Signaling.Immune network · 2025Article
- Cellular senescence and polycystic ovary syndrome: mechanisms and therapeutic strategies from a new perspective.Annals of medicine · 2025Review
- Sleep disorders in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Review
- Association between a history of hypothyroidism and incident chronic kidney disease and potential mediators: A cohort study with Mendelian randomization analysis.The Journal of international medical research · 2025Article
- Targeting HMGCS2: Ketogenesis Suppression Accelerates NAFLD Progression in T2DM Comorbidity, While Cynaroside Ameliorates NASH in Concomitant T2DM.Biomolecules · 2025Article
- Exploring the impact of sleep duration and sleep disorders on metabolic dysfunction-associated steatotic liver disease in older adults.BMC geriatrics · 2025Article
- Therapeutic potential of young plasma in reversing age-related liver inflammation via modulation of NLRP3 inflammasome and necroptosis.Biogerontology · 2025Article
- Bioinformatics-Guided Experimental Validation Identifies NQO1 as a Senescence-Ferroptosis Hub in Liver Fibrosis.Biomedicines · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ageing is an inevitable and multifaceted biological process that impacts a wide range of cellular and molecular mechanisms, leading to the development of various diseases, such as liver fibrosis. Liver fibrosis progresses to cirrhosis, which is an advanced form due to high amounts of extracellular matrix and restoration of normal liver structure with failure to repair damaged tissue and cells, marking the end of liver function and total liver failure, ultimately death. The most important factors are reactive oxygen species (ROS) and cellular senescence. Oxidative stress is defined as an impairment by ROS, which are by-products of the mitochondrial electron transport chain and other key molecular pathways that induce cell damage and can activate cellular senescence pathways. Cellular senescence is characterized by pro-inflammatory cytokines, growth factors, and proteases secreted by senescent cells, collectively known as the senescence-associated secretory phenotype (SASP). The presence of senescent cells, which disrupt tissue architecture and function and increase senescent cell production in liver tissues, contributes to fibrogenesis. Hepatic stellate cells (HSCs) are activated in response to chronic liver injury, oxidative stress, and senescence signals that drive excessive production and deposition of extracellular matrix. This review article aims to provide a comprehensive overview of the pathogenic role of ROS and cellular senescence in the aging liver and their contribution to fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.