ReviewCell death discovery2024
Cellular senescence of renal tubular epithelial cells in acute kidney injury.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed.
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Herpes simplex virus type 2 induces S-phase entry and arrest to regulate the cell cycle for efficient replication.The Journal of general virology · 2026Article
- TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- SGLT2 Inhibition Attenuates Renal Tubular Senescence by Suppressing CTRP1-Mediated Glucotoxic Stress in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Deciphering the impact ofGenes & diseases · 2026Article
- uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2026Review
- A new cancer progression model: From synthetic tumors to real data and back.PLoS computational biology · 2026Article
- Zinc Signaling in Acute Kidney Injury.Cells · 2026Review
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Inhibition of MyD88 in Tubular Epithelial Cells Alleviates the Cellular Senescence in Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Maternal obesity induces macrophage to myofibroblast transition in kidneys of male offspring through a pathway driven by 20-hydroxyeicosatetraenoic acid.Nature communications · 2026Article
- Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Review
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- UBC9-mediated p53 SUMOylation drives tubular senescence and exacerbates acute kidney injury in mice.Acta pharmacologica Sinica · 2026Article
- SASP-driven vascular aging: unraveling the transcriptional nexus in endothelial senescence and cardiovascular disease.Histochemistry and cell biology · 2026Review
- Dual Roles and Therapeutic Prospects of Proximal Tubular Epithelial Cell Senescence in Acute Kidney Injury.Biomolecules · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Cellular senescence represents an irreversible state of cell-cycle arrest during which cells secrete senescence-associated secretory phenotypes, including inflammatory factors and chemokines. Additionally, these cells exhibit an apoptotic resistance phenotype. Cellular senescence serves a pivotal role not only in embryonic development, tissue regeneration, and tumor suppression but also in the pathogenesis of age-related degenerative diseases, malignancies, metabolic diseases, and kidney diseases. The senescence of renal tubular epithelial cells (RTEC) constitutes a critical cellular event in the progression of acute kidney injury (AKI). RTEC senescence inhibits renal regeneration and repair processes and, concurrently, promotes the transition of AKI to chronic kidney disease via the senescence-associated secretory phenotype. The mechanisms underlying cellular senescence are multifaceted and include telomere shortening or damage, DNA damage, mitochondrial autophagy deficiency, cellular metabolic disorders, endoplasmic reticulum stress, and epigenetic regulation. Strategies aimed at inhibiting RTEC senescence, targeting the clearance of senescent RTEC, or promoting the apoptosis of senescent RTEC hold promise for enhancing the renal prognosis of AKI. This review primarily focuses on the characteristics and mechanisms of RTEC senescence, and the impact of intervening RTEC senescence on the prognosis of AKI, aiming to provide a foundation for understanding the pathogenesis and providing potentially effective approaches for AKI treatment.
Identifiers
What OpenQuestion holds
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.