Evidence map›Paper›PMID 22178605›Full record

ArticleBiochimica et biophysica acta2012

Damage to mitochondrial complex I during cardiac ischemia reperfusion injury is reduced indirectly by anti-anginal drug ranolazine.

Ashish K Gadicherla, David F Stowe, William E Antholine, Meiying Yang, Amadou K S Camara

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 83 citations in OpenAlex.

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  15. Oxidative Stress-Responsive MicroRNAs in Heart Injury.International journal of molecular sciences · 2020
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  19. Deactivation of mitochondrial complex I after hypoxia-ischemia in the immature brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Ashish K GadicherlaDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
David F Stowe
William E Antholine
Meiying Yang
Amadou K S Camara
Medical College of Wisconsin · USMarquette University · US

Funding

Cations and ROS in Modulating Mitochondrial Function in Normal and Ischemic HeartR01HL095122 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI CAMARA, AMADOU K., DASH, RANJAN K · 2010 to 2013
$2.1M
Mitochondrial Ca-sensitive K channel-induced superoxide and cardiac protectionR01HL089514 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STOWE, DAVID F · 2009 to 2012
$1.4M
NHLBI NIH HHS R01 HL089514NHLBI NIH HHS R01 HL095122
6 · The paper itself

Abstract

Ranolazine, an anti-anginal drug, is a late Na(+) channel current blocker that is also believed to attenuate fatty acid oxidation and mitochondrial respiratory complex I activity, especially during ischemia. In this study, we investigated if ranolazine's protective effect against cardiac ischemia/reperfusion (IR) injury is mediated at the mitochondrial level and specifically if respiratory complex I (NADH Ubiquinone oxidoreductase) function is protected. We treated isolated and perfused guinea pig hearts with ranolazine just before 30 min ischemia and then isolated cardiac mitochondria at the end of 30 min ischemia and/or 30 min ischemia followed by 10 min reperfusion. We utilized spectrophotometric and histochemical techniques to assay complex I activity, Western blot analysis for complex I subunit NDUFA9, electron paramagnetic resonance for activity of complex I Fe-S clusters, enzyme linked immuno sorbent assay (ELISA) for determination of protein acetylation, native gel histochemical staining for respiratory supercomplex assemblies, and high pressure liquid chromatography for cardiolipin integrity; cardiac function was measured during IR. Ranolazine treated hearts showed higher complex I activity and greater detectable complex I protein levels compared to untreated IR hearts. Ranolazine treatment also led to more normalized electron transfer via Fe-S centers, supercomplex assembly and cardiolipin integrity. These improvements in complex I structure and function with ranolazine were associated with improved cardiac function after IR. However, these protective effects of ranolazine are not mediated by a direct action on mitochondria, but rather indirectly via cytosolic mechanisms that lead to less oxidation and better structural integrity of complex I.

Indexed as

AcetanilidesAnimalsBlotting, WesternCardiolipinsElectron TransportElectron Transport Complex IGuinea PigsMitochondria, HeartMyocardial Reperfusion InjuryPiperazinesRanolazineReactive Oxygen SpeciesAcetanilidesCardiolipinsElectron Transport Complex IPiperazinesRanolazineReactive Oxygen Species

Identifiers

PMID22178605
PMCPMC3269517
OpenAlexW2173575229

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.