ArticleAmerican journal of physiology. Cell physiology2012
Regulation of acid-base transporters by reactive oxygen species following mitochondrial fragmentation.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- A Unified Framework for Spinal Cord Injury Repair: Metabolic-Nutritional Microenvironment Remodeling, Immune Modulation, and Neural Regeneration.Molecular neurobiology · 2026Review
- Cortistatin as a modulator of inflammatory and mitochondrial dysfunction in Huntington´s disease.Journal of neuroinflammation · 2026Article
- Mitochondrial superoxide regulates nuclear envelope integrity and ageing via redox-mediated lipid metabolism.Nature metabolism · 2026Article
- A proton-inhibited DEG/ENaC ion channel maintains neuronal ionstasis and promotes neuronal survival under stress.iScience · 2023Article
- Ethyl isopropyl amiloride decreases oxidative phosphorylation and increases mitochondrial fusion in clonal untransformed and cancer cells.American journal of physiology. Cell physiology · 2021Article
- The Interplay between Dysregulated Ion Transport and Mitochondrial Architecture as a Dangerous Liaison in Cancer.International journal of molecular sciences · 2021Review
- In Vivo Imaging with Genetically Encoded Redox Biosensors.International journal of molecular sciences · 2020Review
- Reactive Oxygen Species-Related Nanoparticle Toxicity in the Biomedical Field.Nanoscale research letters · 2020Review
- Impact of pharmacological agents on mitochondrial function: a growing opportunity?Biochemical Society transactions · 2019Review
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- Regulated spatial organization and sensitivity of cytosolic protein oxidation in Caenorhabditis elegans.Nature communications · 2014Article
- Analysis of Ca2+ signaling motifs that regulate proton signaling through the Na+/H+ exchanger NHX-7 during a rhythmic behavior in Caenorhabditis elegans.The Journal of biological chemistry · 2013Article
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- Mitochondrial network in the heart.Protein & cell · 2012Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial morphology is determined by the balance between the opposing processes of fission and fusion, each of which is regulated by a distinct set of proteins. Abnormalities in mitochondrial dynamics have been associated with a variety of diseases, including neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, and dominant optic atrophy. Although the genetic determinants of fission and fusion are well recognized, less is known about the mechanism(s) whereby altered morphology contributes to the underlying pathophysiology of these disease states. Previous work from our laboratory identified a role for mitochondrial dynamics in intracellular pH homeostasis in both mammalian cell culture and in the genetic model organism Caenorhabditis elegans. Here we show that the acidification seen in mutant animals that have lost the ability to fuse their mitochondrial inner membrane occurs through a reactive oxygen species (ROS)-dependent mechanism and can be suppressed through the use of pharmacological antioxidants targeted specifically at the mitochondrial matrix. Physiological approaches examining the activity of endogenous mammalian acid-base transport proteins in rat liver Clone 9 cells support the idea that ROS signaling to sodium-proton exchangers contributes to acidification. Because maintaining pH homeostasis is essential for cell function and viability, the results of this work provide new insight into the pathophysiology associated with the loss of inner mitochondrial membrane fusion.
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Registered trials
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