ArticleOncotarget2016
Apoptotic transition of senescent cells accompanied with mitochondrial hyper-function.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 21 citations in OpenAlex.
- ACSS2-KAT5 complex-driven histone crotonylation orchestrates a pro-inflammatory program to promote the transition from MASLD to MASH.Nature communications · 2026Article
- Article
- β-Catenin and AMPK/AKT/FOXO Signaling Mediate Doxorubicin-Induced Senescence and Lipid Accumulation in C2C12 Myoblasts.Biomolecules & therapeutics · 2026Article
- Systemic comparison of molecular characteristics in different skin fibroblast senescent models.Chinese medical journal · 2025Article
- YPEL3 expression induces cellular senescence via the Hippo signaling pathway in human breast cancer cells.Toxicological research · 2023Article
- Riboflavin transporter SLC52A1, a target of p53, suppresses cellular senescence by activating mitochondrial complex II.Molecular biology of the cell · 2021Article
- Structural and Functional Remodeling of Mitochondria in Cardiac Diseases.International journal of molecular sciences · 2021Review
- Tissue Nonspecific Alkaline Phosphatase Function in Bone and Muscle Progenitor Cells: Control of Mitochondrial Respiration and ATP Production.International journal of molecular sciences · 2021Article
- Agent-Based Models Predict Emergent Behavior of Heterogeneous Cell Populations in Dynamic Microenvironments.Frontiers in bioengineering and biotechnology · 2020Article
- Senescence and Apoptosis DuringFrontiers in cell and developmental biology · 2020Review
- Impact of pharmacological agents on mitochondrial function: a growing opportunity?Biochemical Society transactions · 2019Review
- Short exposure to cold atmospheric plasma induces senescence in human skin fibroblasts and adipose mesenchymal stromal cells.Scientific reports · 2019Article
- Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts.GeroScience · 2018Article
- Polymorphism rs1385129 Within Glut1 GeneFrontiers in immunology · 2018Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defined as stable cell-cycle arrest, cellular senescence plays an important role in diverse biological processes including tumorigenesis, organismal aging, and embryonic development. Although increasing evidence has documented the metabolic changes in senescent cells, mitochondrial function and its potential contribution to the fate of senescent cells remain largely unknown. Here, using two in vitro models of cellular senescence induced by doxorubicin treatment and prolonged passaging of neonatal human foreskin fibroblasts, we report that senescent cells exhibited high ROS level and augmented glucose metabolic rate concomitant with both morphological and quantitative changes of mitochondria. Furthermore, mitochondrial membrane potential depolarized at late stage of senescent cells which eventually led to apoptosis. Our study reveals that mitochondrial hyper-function contributes to the implementation of cellular senescence and we propose a model in which the mitochondrion acts as the key player in promoting fate-determination in senescent cells.
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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.