Evidence map›Paper›PMID 25392542›Full record

ArticleJournal of the American Heart Association2014

Mitochondrial aldehyde dehydrogenase activation by Alda-1 inhibits atherosclerosis and attenuates hepatic steatosis in apolipoprotein E-knockout mice.

Aneta Stachowicz, Rafał Olszanecki, Maciej Suski, Anna Wiśniewska, Justyna Totoń-Żurańska, Józef Madej, Jacek Jawień, Magdalena Białas, Krzysztof Okoń, Mariusz Gajda and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Trimethylamine oxide induces pyroptosis of vascular endothelial cells through ALDH2/ROS/NLRP3/GSDMD pathway.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Aldehyde Dehydrogenase, Liver Disease and Cancer.International journal of biological sciences · 2020
    Review
  15. Article
  16. Article
  17. Diesel Exhaust Induces Mitochondrial Dysfunction, Hyperlipidemia, and Liver Steatosis.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  18. Crude α-Mangostin Suppresses the Development of Atherosclerotic Lesions inInternational journal of molecular sciences · 2019
    Article
  19. 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

13 authors at 3 institutions in 1 country.

Aneta StachowiczDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Rafał OlszaneckiDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Maciej SuskiDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Anna WiśniewskaDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Justyna Totoń-ŻurańskaDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Józef MadejDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Jacek JawieńDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Magdalena BiałasDepartment of Pathomorphology, Jagiellonian University Medical College, Krakow, Poland (M.B., K.O.).
Krzysztof OkońDepartment of Pathomorphology, Jagiellonian University Medical College, Krakow, Poland (M.B., K.O.).
Mariusz GajdaDepartment of Histology, Jagiellonian University Medical College, Krakow, Poland (M.G.).
Katarzyna GłombikDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland (K., A.B.K.).
Agnieszka Basta-KaimDepartment of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland (K., A.B.K.).
Ryszard KorbutDepartment of Pharmacology, Jagiellonian University Medical College, Krakow, Poland (A.S., R.O., M.S., A.W., J.T., M., J.J., R.K.).
Jagiellonian University · PLMaj Institute of Pharmacology · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial dysfunction has been shown to play an important role in the development of atherosclerosis and nonalcoholic fatty liver disease (NAFLD). Mitochondrial aldehyde dehydrogenase (ALDH2), an enzyme responsible for the detoxification of reactive aldehydes, is considered to exert protective function in mitochondria. We investigated the influence of Alda-1, an activator of ALDH2, on atherogenesis and on the liver steatosis in apolipoprotein E knockout (apoE(-/-)) mice. METHODS AND

resultsAlda-1 caused decrease of atherosclerotic lesions approximately 25% as estimated by "en face" and "cross-section" methods without influence on plasma lipid profile, atherosclerosis-related markers of inflammation, and macrophage and smooth muscle content in the plaques. Plaque nitrotyrosine was not changed upon Alda-1 treatment, and there were no changes in aortic mRNA levels of factors involved in antioxidative defense, regulation of apoptosis, mitogenesis, and autophagy. Hematoxylin/eosin staining showed decrease of steatotic changes in liver of Alda-1-treated apoE(-/-) mice. Alda-1 attenuated formation of 4-hydroxy-2-nonenal (4-HNE) protein adducts and decreased triglyceride content in liver tissue. Two-dimensional electrophoresis coupled with mass spectrometry identified 20 differentially expressed mitochondrial proteins upon Alda-1 treatment in liver of apoE(-/-) mice, mostly proteins related to metabolism and oxidative stress. The most up-regulated were the proteins that participated in beta oxidation of fatty acids.

conclusionsCollectively, Alda-1 inhibited atherosclerosis and attenuated NAFLD in apoE(-/-) mice. The pattern of changes suggests a beneficial effect of Alda-1 in NAFLD; however, the exact liver functional consequences of the revealed alterations as well as the mechanism(s) of antiatherosclerotic Alda-1 action require further investigation.

Indexed as

Aldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisBenzamidesBenzodioxolesBiomarkersDisease Models, AnimalEnzyme ActivationEnzyme ActivatorsFemaleGene Expression RegulationHep G2 CellsAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, mouseApolipoproteins EBenzamidesBenzodioxolesBiomarkersEnzyme ActivatorsN-(1,3-benzodioxol-5-ylmethyl)-2,6-dichlorobenzamideAlda‐1ALDH2atherosclerosismitochondrianonalcoholic fatty liver disease

Identifiers

PMID25392542
PMCPMC4338726
OpenAlexW2143831767

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.