ArticleIEEE journal of translational engineering in health and medicine2021
Optical Metabolic Imaging of Mitochondrial Dysfunction on HADH Mutant Newborn Rat Hearts.
Article in IEEE journal of translational engineering in health and medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Single-cell metabolic profiling of stallion spermatozoa by flow cytometry using NADH and FAD autofluorescence†.Biology of reproduction · 2026Article
- A nuclear isoform of hydroxyacyl-COA dehydrogenase inhibits tumor progression in colorectal cancer.iScience · 2026Article
- Screening of circRNAs Associated with Secondary Wool Follicle Development in Fine-Wool Sheep and Construction of Their ceRNA Network.Animals : an open access journal from MDPI · 2025Article
- CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress.Frontiers in cardiovascular medicine · 2025Article
- Morphine induces HADHA succinylation, while HADHA desuccinylation alleviates morphine tolerance by influencing autophagy.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2024Article
- Accurate phenotypic classification and exome sequencing allow identification of novel genes and variants associated with adult-onset hearing loss.PLoS genetics · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
backgroundMitochondrial [Formula: see text]-oxidation of fatty acids is the primary energy source for the heart and carried out by Hydroxy Acyl-CoA Dehydrogenase (HADH) encoded trifunctional protein. Mutations in the genes encoding mitochondrial proteins result in functionally defective protein complexes that contribute to energy deficiencies, excessive reactive oxygen species (ROS) production, and accumulation of damaged mitochondria. We hypothesize that a dramatic alternation in redox state and associated mitochondrial dysfunction is the underlying cause of Fatty Acid Oxidation (FAO) deficiency mutant, resulting in heart failure. Mitochondrial co-enzymes, NADH and FAD, are autofluorescent metabolic indices of cells when imaged, yield a quantitative assessment of the cells' redox status and, in turn, that of the tissue and organ.
methodWe utilized an optical cryo-imager to quantitively evaluate the three-dimensional distribution of mitochondrial redox state in newborn rats' hearts and kidneys. Redox ratio (RR) assessment shows that mitochondrial dysfunction is extreme and could contribute to severe heart problems and eventual heart failure in the mutants.
resultsThree-dimensional redox ratio (NADH/FAD) rendering, and the volumetric mean value calculations confirmed significantly decreased cardiac RR in mutants by 31.90% and 12.32%, in renal mitochondrial RR compared to wild-type control. Further, histological assessment of newborn heart myocardial tissue indicated no significant difference in myocardial tissue architecture in both control and severe (HADHA
conclusionThese results demonstrate that optical imaging can accurately estimate the redox state changes in newborn rat organs. It is also apparent that the FAO mutant's heart tissue with a low redox ratio is probably more vulnerable to cumulative damages than kidneys and fails prematurely, contributing to sudden death.
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