ReviewTranslational stroke research2018
Significance of Mitochondrial Protein Post-translational Modifications in Pathophysiology of Brain Injury.
Review in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 33 citations in OpenAlex.
- Inhibition of PKCγ phosphorylation protects against cerebral ischemia-reperfusion injury.Redox biology · 2026Article
- The UBC/SIRT5/DRP1 axis regulates mitochondrial dynamics to alleviate Staphylococcus aureus-induced oxidative stress and senescence in bovine mammary epithelial cells.PLoS pathogens · 2026Article
- Sexual Dimorphism of Ethanol-Induced Mitochondrial Dynamics in Purkinje Cells.International journal of molecular sciences · 2024Article
- The mitochondria as a potential therapeutic target in cerebral I/R injury.Frontiers in neuroscience · 2024Review
- Bendless is essential for PINK1-Park mediated Mitofusin degradation under mitochondrial stress caused by loss of LRPPRC.PLoS genetics · 2023Article
- Deep Succinylproteomics of Brain Tissues from Intracerebral Hemorrhage with Inhibition of Toll-Like Receptor 4 Signaling.Cellular and molecular neurobiology · 2022Article
- Rethinking the necessity of low glucose intervention for cerebral ischemia/reperfusion injury.Neural regeneration research · 2022Review
- Brain ethanol metabolism and mitochondria.Current topics in biochemical research · 2022Article
- Article
- PTMs: A Missing Piece for Schizophrenia Studies.Advances in experimental medicine and biology · 2022Article
- Review
- A Novel Role of Claudin-5 in Prevention of Mitochondrial Fission Against Ischemic/Hypoxic Stress in Cardiomyocytes.The Canadian journal of cardiology · 2021Article
- Sodium butyrate attenuated neuronal apoptosis via GPR41/Gβγ/PI3K/Akt pathway after MCAO in rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Article
- Role of NADBrain sciences · 2020Review
- Mechanisms and roles of mitochondrial localisation and dynamics in neuronal function.Neuronal signaling · 2020Review
- NADExperimental neurology · 2020Review
- Mst1 Knockout Alleviates Mitochondrial Fission and Mitigates Left Ventricular Remodeling in the Development of Diabetic Cardiomyopathy.Frontiers in cell and developmental biology · 2020Article
- Mitochondrial Quality Control in Cardiomyocytes: A Critical Role in the Progression of Cardiovascular Diseases.Frontiers in physiology · 2020Review
- Multi-targeted Effect of Nicotinamide Mononucleotide on Brain Bioenergetic Metabolism.Neurochemical research · 2019Review
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 1 country.
Funding
Abstract
Mitochondria are complex organelles that undergo constant fusion and fission in order to adapt to the ever-changing cellular environment. The fusion/fission proteins, localized in the inner and outer mitochondrial membrane, play critical roles under pathological conditions such as acute brain injury and neurodegenerative diseases. Post-translational modifications of these proteins tightly regulate their function and activity, ultimately impacting mitochondrial dynamics and their efficiency to generate ATP. The individual post-translational modifications that are known to affect mitochondrial dynamics include SUMOylation, ubiquitination, phosphorylation, S-nitrosylation, acetylation, O-linked N-acetyl-glucosamine glycosylation, ADP-ribosylation, and proteolytic cleavage. Under stress or pathologic conditions, several of these modifications are activated leading to a complex regulatory mechanism that shifts the state of the mitochondrial network. The main goal is to accommodate and adapt the cellular bioenergetics metabolism to the energetic demand of the new extra- and/or intracellular environment. Understanding the complex relationship between these modifications on fusion and fission proteins in particular pathologic stress or diseases can provide new promising therapeutic targets and treatment approaches. Here, we discuss the specific post-translational modifications of mitochondrial fusion/fission proteins under pathologic conditions and their impact on mitochondrial dynamics.
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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.