ReviewEBioMedicine2017
Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?
Review in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 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
229 citing papers in PubMed, 383 citations in OpenAlex.
- The cGAS-STING pathway in inflammaging and neuroinflammation.Science China. Life sciences · 2026Review
- Resveratroloside alleviates senescence-associated phenotypes in vitro through the coordinated regulation of mitochondrial function and chromatin structure.Biogerontology · 2026Article
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Pyrroloquinoline Quinone (PQQ) as a Mitochondrial Rejuvenation Strategy in Aesthetic Dermatology: Mechanisms, Therapeutic Potential, and Future Clinical Applications.Biomolecules · 2026Review
- Review
- Sensory decline in aging and neurodegeneration: A mitochondrial perspective.Pharmacological research · 2026Review
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Progranulin deficiency induces premature vascular senescence and dysfunction.American journal of physiology. Heart and circulatory physiology · 2026Article
- TIA-1 promotes FUNDC1-mediated mitophagy to protect against stress-induced cellular senescence.Experimental & molecular medicine · 2026Article
- Therapeutic Potential of miR-196a in Protecting Corneal Endothelial Cells From Senescence Through Mitochondrial and TGF-β Signaling Modulation.Translational vision science & technology · 2026Article
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- Modulation of Iron-Induced Glucose Metabolic Reprogramming Alleviates Retinal Pigment Epithelial Cell Senescence.Investigative ophthalmology & visual science · 2026Article
- Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.BMB reports · 2026Review
- FTO-dependent m6A methylation mediates gestational diabetes mellitus-induced offspring cardiac senescent hypertrophy and dysfunction.iScience · 2026Article
- Mitochondrial transfer in the tumor microenvironment: a dynamic determinant of cancer plasticity, immune dysfunction, and therapeutic opportunity.Frontiers in immunology · 2026Review
- PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence.Research (Washington, D.C.) · 2026Article
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Regulatory mechanisms and interactions of mitophagy and ketone body metabolism in cardiac metabolism.Frontiers in cardiovascular medicine · 2026Review
- AUF1 Restrains Hepatocyte Senescence by Maintaining Mitochondrial Homeostasis in AML12 Hepatocyte Model.Cells · 2025Article
- The Immunoregulatory Mechanisms of Human Cytomegalovirus from Primary Infection to Reactivation.Pathogens (Basel, Switzerland) · 2025Review
169 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Cell senescence is increasingly recognized as a major contributor to the loss of health and fitness associated with aging. Senescent cells accumulate dysfunctional mitochondria; oxidative phosphorylation efficiency is decreased and reactive oxygen species production is increased. In this review we will discuss how the turnover of mitochondria (a term referred to as mitophagy) is perturbed in senescence contributing to mitochondrial accumulation and Senescence-Associated Mitochondrial Dysfunction (SAMD). We will further explore the subsequent cellular consequences; in particular SAMD appears to be necessary for at least part of the specific Senescence-Associated Secretory Phenotype (SASP) and may be responsible for tissue-level metabolic dysfunction that is associated with aging and obesity. Understanding the complex interplay between these major senescence-associated phenotypes will help to select and improve interventions that prolong healthy life in humans. SEARCH STRATEGY AND SELECTION CRITERIA: Data for this review were identified by searches of MEDLINE, PubMed, and references from relevant articles using the search terms "mitochondria AND senescence", "(autophagy OR mitophagy) AND senescence", "mitophagy AND aging" and related terms. Additionally, searches were performed based on investigator names. Abstracts and reports from meetings were excluded. Articles published in English between 1995 and 2017 were included. Articles were selected according to their relevance to the topic as perceived by the authors.
Indexed as
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.