ArticleAdipocyte2013
New roles for OMA1 metalloprotease: From mitochondrial proteostasis to metabolic homeostasis.
Article in Adipocyte, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Adipose Tissue-Central Nervous System Axis in Obesity: Molecular Mechanisms, Inflammation, and Nutritional and Technological Implications.Metabolites · 2026Review
- Age-related changes in energy metabolism in peripheral mononuclear blood cells (PBMCs) and the brains of cognitively healthy seniors.GeroScience · 2024Observational
- High-fat diet causes mitochondrial damage and downregulation of mitofusin-2 and optic atrophy-1 in multiple organs.Journal of clinical biochemistry and nutrition · 2023Article
- The regulatory role of adipocyte mitochondrial homeostasis in metabolism-related diseases.Frontiers in physiology · 2023Review
- Chronic Exercise Improves Mitochondrial Function and Insulin Sensitivity in Brown Adipose Tissue.Frontiers in physiology · 2018Article
- Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2017Review
- New roles for mitochondrial proteases in health, ageing and disease.Nature reviews. Molecular cell biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial quality control system is essential for the preservation and regulation of mitochondrial function. This system is formed by a complex machinery that controls and maintains protein function and regulates mitochondrial morphology through a coordinated system of continual fusion and fission events. Impairments in the mitochondrial quality control system through either mutation or deficiency in any of its components, can lead to mitochondrial dysfunction. However, the physiological consequences of these deficiencies remain unknown in most cases. Here, we briefly review the role of the OPA1-OMA1 system in mitochondrial biology, and summarize our recent report on the generation and phenotypic characterization of a model deficient in OMA1, an ATP-independent mitochondrial metalloprotease that participates in mitochondrial quality control. Interestingly,
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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.