ArticleCell death and differentiation2017
Ageing and hypoxia cause protein aggregation in mitochondria.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Raptor and Drp1 Function Synthetically to Control Hypoxic Death and the Mitochondrial Network in Caenorhabditis elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer's-like neuropathology.Basic research in cardiology · 2025Article
- Mechanisms of the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans and Mammals and Its Roles in Striated Muscles.Aging and disease · 2024Review
- Protein aggregation and biomolecular condensation in hypoxic environments (Review).International journal of molecular medicine · 2024Review
- Article
- Hypoxia-induced mitochondrial stress granules.Cell death & disease · 2023Article
- Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- SIAH proteins regulate the degradation and intra-mitochondrial aggregation of PINK1: Implications for mitochondrial pathology in Parkinson's disease.Aging cell · 2022Article
- Estimation of Caenorhabditis Elegans Lifespan Stages Using a Dual-Path Network Combining Biomarkers and Physiological Changes.Bioengineering (Basel, Switzerland) · 2022Article
- Logic of the Temporal Compartmentalization of the Hepatic Metabolic Cycle.Physiology (Bethesda, Md.) · 2022Review
- Daf-16 mediated repression of cytosolic ribosomal protein genes facilitates a hypoxia sensitive to hypoxia resistant transformation in long-lived germline mutants.PLoS genetics · 2022Article
- Autophagy and the Bone Marrow Microenvironment: A Review of Protective Factors in the Development and Maintenance of Multiple Myeloma.Frontiers in immunology · 2022Review
- Mitochondrial dysfunction, UPRCell & bioscience · 2021Review
- Protein Aggregation in the Pathogenesis of Ischemic Stroke.Cellular and molecular neurobiology · 2021Review
- Effect of the mitochondrial unfolded protein response on hypoxic death and mitochondrial protein aggregation.Cell death & disease · 2021Article
- Review
- Regulating glycolysis and heat shock proteins in Gannan yaks (Archives animal breeding · 2021Article
- Mitochondrial Stress Response and Cancer.Trends in cancer · 2020Review
- Hypoxia-Induced Degenerative Protein Modifications Associated with Aging and Age-Associated Disorders.Aging and disease · 2020Review
- A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Aggregation of cytosolic proteins is a pathological finding in disease states, including ageing and neurodegenerative diseases. We have previously reported that hypoxia induces protein misfolding in Caenorhabditis elegans mitochondria, and electron micrographs suggested protein aggregates. Here, we seek to determine whether mitochondrial proteins actually aggregate after hypoxia and other cellular stresses. To enrich for mitochondrial proteins that might aggregate, we performed a proteomics analysis on purified C. elegans mitochondria to identify relatively insoluble proteins under normal conditions (110 proteins identified) or after sublethal hypoxia (65 proteins). A GFP-tagged mitochondrial protein (UCR-11 - a complex III electron transport chain protein) in the normally insoluble set was found to form widespread aggregates in mitochondria after hypoxia. Five other GFP-tagged mitochondrial proteins in the normally insoluble set similarly form hypoxia-induced aggregates. Two GFP-tagged mitochondrial proteins from the soluble set as well as a mitochondrial-targeted GFP did not form aggregates. Ageing also resulted in aggregates. The number of hypoxia-induced aggregates was regulated by the mitochondrial unfolded protein response (UPRmt) master transcriptional regulator ATFS-1, which has been shown to be hypoxia protective. An atfs-1(loss-of-function) mutant and RNAi construct reduced the number of aggregates while an atfs-1(gain-of-function) mutant increased aggregates. Our work demonstrates that mitochondrial protein aggregation occurs with hypoxic injury and ageing in C. elegans. The UPRmt regulates aggregation and may protect from hypoxia by promoting aggregation of misfolded proteins.
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.