ArticleFree radical biology & medicine2017
Administration of 5-methoxyindole-2-carboxylic acid that potentially targets mitochondrial dihydrolipoamide dehydrogenase confers cerebral preconditioning against ischemic stroke injury.
Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Compression-induced metabolic adaptation drives confined tumor cell migration and distant metastasis via malate-dependent microtubule reinforcement.Cell research · 2026Article
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024Review
- Roles of Dihydrolipoamide Dehydrogenase in Health and Disease.Antioxidants & redox signaling · 2023Review
- Renal-Protective Roles of Lipoic Acid in Kidney Disease.Nutrients · 2023Review
- The pathogenesis of DLD-mediated cuproptosis induced spinal cord injury and its regulation on immune microenvironment.Frontiers in cellular neuroscience · 2023Article
- Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NADBiomolecules · 2022Review
- Cadmium-Induced Kidney Injury: Oxidative Damage as a Unifying Mechanism.Biomolecules · 2021Review
- 5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.Reactive oxygen species (Apex, N.C.) · 2020Article
- Effects of dietary 5-methoxyindole-2-carboxylic acid on brain functional recovery after ischemic stroke.Behavioural brain research · 2020Article
- Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges.Frontiers in neurology · 2020Review
- Chronic Inhibition of Mitochondrial Dihydrolipoamide Dehydrogenase (DLDH) as an Approach to Managing Diabetic Oxidative Stress.Antioxidants (Basel, Switzerland) · 2019Article
- Critical Role of Nrf2 in Experimental Ischemic Stroke.Frontiers in pharmacology · 2019Review
- Post-ischemic administration of 5-methoxyindole-2-carboxylic acid at the onset of reperfusion affords neuroprotection against stroke injury by preserving mitochondrial function and attenuating oxidative stress.Biochemical and biophysical research communications · 2018Article
- Reexploring 5-methoxyindole-2-carboxylic acid (MICA) as a potential antidiabetic agent.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The objective of this study was to investigate a possible role of mitochondrial dihydrolipoamide dehydrogenase (DLDH) as a chemical preconditioning target for neuroprotection against ischemic injury. We used 5-methoxyindole-2-carboxylic acid (MICA), a reportedly reversible DLDH inhibitor, as the preconditioning agent and administered MICA to rats mainly via dietary intake. Upon completion of 4 week's MICA treatment, rats underwent 1h transient ischemia and 24h reperfusion followed by tissue collection. Our results show that MICA protected the brain against ischemic stroke injury as the infarction volume of the brain from the MICA-treated group was significantly smaller than that from the control group. Data were then collected without or with stroke surgery following MICA feeding. It was found that in the absence of stroke following MICA feeding, DLDH activity was lower in the MICA treated group than in the control group, and this decreased activity could be partly due to DLDH protein sulfenation. Moreover, DLDH inhibition by MICA was also found to upregulate the expression of NAD(P)H-ubiquinone oxidoreductase 1(NQO1) via the Nrf2 signaling pathway. In the presence of stroke following MICA feeding, decreased DLDH activity and increased Nrf2 signaling were also observed along with increased NQO1 activity, decreased oxidative stress, decreased cell death, and increased mitochondrial ATP output. We also found that MICA had a delayed preconditioning effect four weeks post MICA treatment. Our study indicates that administration of MICA confers chemical preconditioning and neuroprotection against ischemic stroke injury.
Indexed as
Identifiers
What OpenQuestion holds
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.