ArticleRedox biology2018
Cardiac-specific overexpression of aldehyde dehydrogenase 2 exacerbates cardiac remodeling in response to pressure overload.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Matricellular protein CCN1 promotes collagen alignment and scar integrity after myocardial infarction.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Repurposing of an antiasthmatic drug may reduce NETosis and myocardial ischaemia/reperfusion injury.European heart journal · 2024Article
- Visfatin aggravates transverse aortic constriction-induced cardiac remodelling by enhancing macrophage-mediated oxidative stress in mice.Journal of cellular and molecular medicine · 2023Article
- Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overload.American journal of physiology. Heart and circulatory physiology · 2021Article
- Alpha-lipoic acid protects against pressure overload-induced heart failure via ALDH2-dependent Nrf1-FUNDC1 signaling.Cell death & disease · 2020Article
- An emerging perspective on sex differences: Intersecting S-nitrosothiol and aldehyde signaling in the heart.Redox biology · 2020Review
- E2f1 deletion attenuates infarct-induced ventricular remodeling without affecting O-GlcNAcylation.Basic research in cardiology · 2019Article
- [Mitochondrial aldehyde dehydrogenase 2 protects against high glucose-induced injury in neonatal rat cardiomyocytes by regulating CaN-NFAT3 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Pathological cardiac remodeling during heart failure is associated with higher levels of lipid peroxidation products and lower abundance of several aldehyde detoxification enzymes, including aldehyde dehydrogenase 2 (ALDH2). An emerging idea that could explain these findings concerns the role of electrophilic species in redox signaling, which may be important for adaptive responses to stress or injury. The purpose of this study was to determine whether genetically increasing ALDH2 activity affects pressure overload-induced cardiac dysfunction. Mice subjected to transverse aortic constriction (TAC) for 12 weeks developed myocardial hypertrophy and cardiac dysfunction, which were associated with diminished ALDH2 expression and activity. Cardiac-specific expression of the human ALDH2 gene in mice augmented myocardial ALDH2 activity but did not improve cardiac function in response to pressure overload. After 12 weeks of TAC, ALDH2 transgenic mice had larger hearts than their wild-type littermates and lower capillary density. These findings show that overexpression of ALDH2 augments the hypertrophic response to pressure overload and imply that downregulation of ALDH2 may be an adaptive response to certain forms of cardiac pathology.
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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.