ArticleCurrent biology : CB2015
Mitochondrial Proteostatic Collapse Leads to Hypoxic Injury.
Article in Current biology : CB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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.
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Who cites it
29 citing papers in PubMed, 32 citations in OpenAlex.
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- Article
- 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
- Targeting Mitochondrial Stress Responses: Terbinafine and Miglustat as Novel Lifespan and Healthspan Modulators.Aging cell · 2026Article
- Mitochondrial dynamics and quality control regulate proteostasis in neuronal ischemia-reperfusion.Autophagy · 2025Article
- Mechanisms of the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans and Mammals and Its Roles in Striated Muscles.Aging and disease · 2024Review
- Decreased ATF5 level contributes to improved mitochondrial function in oocytes exposed to vitrification stress.Frontiers in cell and developmental biology · 2024Article
- Mitochondrial Factors in the Cell Nucleus.International journal of molecular sciences · 2023Review
- Hypoxia-induced mitochondrial stress granules.Cell death & disease · 2023Article
- Evidence From Human Placenta, Endoplasmic Reticulum-Stressed Trophoblasts, and Transgenic Mice Links Transthyretin Proteinopathy to Preeclampsia.Hypertension (Dallas, Tex. : 1979) · 2022Article
- 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
- FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.Autophagy · 2021Article
- Article
- Article
- Effect of the mitochondrial unfolded protein response on hypoxic death and mitochondrial protein aggregation.Cell death & disease · 2021Article
- Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance in C. elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Disruption of mitochondrial dynamics increases stress resistance through activation of multiple stress response pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Alcohol induces mitochondrial fragmentation and stress responses to maintain normal muscle function in Caenorhabditis elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Hypoxia-Induced Degenerative Protein Modifications Associated with Aging and Age-Associated Disorders.Aging and disease · 2020Review
- Mitochondrial Dysfunction and Changes in High-Energy Compounds in Different Cellular Models Associated to Hypoxia: Implication to Schizophrenia.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxic injury is a key pathological event in a variety of diseases. Despite the clinical importance of hypoxia, modulation of hypoxic injury mechanisms for therapeutic benefit has not been achieved, suggesting that critical features of hypoxic injury have not been identified or fully understood. Because mitochondria are the main respiratory organelles of the cell, they have been the focus of much research into hypoxic injury. Previous research has focused on mitochondria as effectors of hypoxic injury, primarily in the context of apoptosis activation and calcium regulation; however, little is known about how mitochondria themselves are injured by hypoxia. Maintenance of protein folding is essential for normal mitochondrial function, whereas failure to maintain protein homeostasis (proteostasis) appears to be a component of aging and a variety of diseases. Previously, it has been demonstrated that mitochondria possess their own unfolded protein response that is activated in response to mitochondrial protein folding stress, a response that is best understood in C. elegans. Because hypoxia has been shown to disrupt ATP production and translation of nuclear encoded proteins--both of which are shown to disrupt mitochondrial proteostasis in other contexts-we hypothesized that failure to maintain mitochondrial proteostasis may play a role in hypoxic injury. Utilizing C. elegans models of global, focal, and cell non-autonomous hypoxic injury, we have found evidence of mitochondrial protein misfolding post-hypoxia and have found that manipulation of the mitochondrial protein folding environment is an effective hypoxia protective strategy.
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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.