ArticleThe EMBO journal2023
TFEB-dependent lysosome biogenesis is required for senescence.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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Who cites it
54 citing papers in PubMed, 62 citations in OpenAlex.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Quantitative proteomics reveals coordinated changes in the proteome during replicative senescence.Nature communications · 2026Article
- Arsenic Inhibits the PA28α/β-PSMB5 Pathway Blocking Phosphorylated TFEB Degradation and Causing Lysosomal Dysfunction that Damages the Liver.Biological trace element research · 2026Article
- Down-Regulation of TFEB With Defective Autophagy in the Susceptibility of Aging Kidneys to Septic Acute Kidney Injury.Aging cell · 2026Article
- Lysosomes and lysosomal dysfunction in ageing biology.Nature cell biology · 2026Review
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Spatial mapping and senolytic targeting of senescent and disease-associated microglia in aged mouse brain white matter.Nature aging · 2026Article
- Article
- Quercetin Mitigates Oxidative Stress-Induced Premature Senescence in SH-SY5Y Neuronal-like Cells.International journal of molecular sciences · 2026Article
- Cell size-dependent mRNA transcription drives proteome remodeling.Cell reports · 2026Article
- Mitochondria-lysosome coupling contributes to lysosome acidification and aging.Molecular cell · 2026Article
- Ferrous Iron Accumulation Is a Hallmark and Therapeutic Vulnerability of Therapy-Induced Senescence.bioRxiv : the preprint server for biology · 2026Article
- Targeting the RNF31-TFEB-NLRP3 Axis With a Curcumin Analog to Restore Autophagy and Alleviate Intestinal Inflammation.Food science & nutrition · 2026Article
- Lysosomal Profiling with LysoTracker for Quantitative Assessment of Cellular Senescence in Human Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- Deruxtecan-based antibody-drug-conjugates induce senescence in HER2-positive breast cancer.Scientific reports · 2026Article
- Elevated lysosomal mass and enzyme activity in fibroblasts of the Mediterranean mouse Mus spretus.Biology letters · 2026Article
- Ginsenoside Rg1 delays the senescence of adipose-derived stem cells: network pharmacology and experimental validation.Hereditas · 2026Article
- Intermittent hypobaric pressure induces selective senescent cell death and alleviates age-related osteoporosis.Nature biomedical engineering · 2026Article
- Defect in lysosomal enzyme trafficking and sorting is associated with irreversibility of pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2026Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The accumulation of senescent cells is recognised as a driver of tissue and organismal ageing. One of the gold-standard hallmarks of a senescent cell is an increase in lysosomal content, as measured by senescence-associated β-galactosidase (Senβ-Gal) activity. The lysosome plays a central role in integrating mitogenic and stress cues to control cell metabolism, which is known to be dysregulated in senescence. Despite this, little is known about the cause and consequence of lysosomal biogenesis in senescence. We find here that lysosomes in senescent cells are dysfunctional; they have higher pH, increased evidence of membrane damage and reduced proteolytic capacity. The significant increase in lysosomal content is however sufficient to maintain degradative capacity of the cell to a level comparable to proliferating control cells. We demonstrate that increased nuclear TFEB/TFE3 supports lysosome biogenesis, is a hallmark of multiple forms of senescence and is required for senescent cell survival. TFEB/TFE3 are hypo-phosphorylated and show constitutive nuclear localisation in senescence. Evidence suggests that several pathways may contribute to TFEB/TFE3 dysregulation in senescence.
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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 Socratic graph.