Evidence map›Paper›PMID 26392772›Full record

ArticleTherapeutics and clinical risk management2015

Aldehyde dehydrogenase-2 protects against myocardial infarction-related cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway.

Xinjun Zhao, Yue Hua, Hongmei Chen, Haiyu Yang, Tao Zhang, Guiqiong Huang, Huijie Fan, Zhangbin Tan, Xiaofang Huang, Bin Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Therapeutics and clinical risk management, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  5. Heart failure, inflammation and exercise.International journal of biological sciences · 2025
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  11. Review
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  13. Article
  14. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  15. Review
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  17. Article
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  19. Review
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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

11 authors at 1 institution in 1 country.

Xinjun ZhaoThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Yue HuaThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Hongmei ChenThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Haiyu YangJiangmen Wuyi Traditional Chinese Medicine Hospital, Guangdong, Jiangmen, People's Republic of China.
Tao ZhangThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Guiqiong HuangHuizhou Hospital of Traditional Chinese Medicine, Huizhou, People's Republic of China.
Huijie FanThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Zhangbin TanThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Xiaofang HuangThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Bin LiuThe Second Affiliated Hospital of Guangzhou Medical University, Guangdong, Guangzhou, People's Republic of China.
Yingchun ZhouThe Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangdong, Guangzhou, People's Republic of China ; Nanfang Hospital, Southern Medical University, Guangdong, Guangzhou, People's Republic of China.
Zero to Three · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAldehyde dehydrogenase-2 (ALDH2) has a protective effect on ischemic heart disease. Here, we examined the protective effects of ALDH2 on cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway in a rat model of myocardial infarction (MI).

methodsWistar rats were divided into the sham (control), MI (model), and ALDH2 activator (Alda-1) groups. After 10 days of treatment, the left ventricular (LV) remodeling parameters of each animal were evaluated by echocardiography. Myocardial fibrosis was evaluated by Masson's trichrome staining and Sirius Red staining. Expression levels of collagen types I and III and α-smooth muscle actin (α-SMA) were examined. Finally, the expression and activity of ALDH2 and the levels of several Wnt-related proteins and genes, such as phosphoglycogen synthase kinase (GSK)-3β, GSK-3β, β-catenin, Wnt-1, WNT1-inducible signaling-pathway protein 1, and tumor necrosis factor (TNF)-α, were also analyzed.

resultsAfter MI, the heart weight/body weight ratio, LV dimension at end diastole, and LV dimension at end systole were decreased, while the LV ejection fraction and LV fractional shortening were increased in the Alda-1 group. Myocardial fibrosis was also reduced in the Alda-1 group, accompanied by decreased expression collagen types I and III and α-SMA. β-Catenin, phosphorylated GSK-3β, and Wnt-1 levels were significantly increased in the model group. Interestingly, this alteration was partly reversed by Alda-1 treatment. Immunohistochemical staining showed that numerous WNT1-inducible signaling-pathway protein 1 (WISP-1)- and TNF-α-positive cells were found in the model group. However, few WISP-1- and TNF-α-positive cells were detected in the Alda-1 group.

conclusionThe reduction of cardiac fibrosis and the down-regulation of β-catenin, phosphorylated GSK-3β, Wnt-1, and WISP-1 may be mediated by increased ALDH2 activity, leading to reduction of MI-related cardiac fibrosis.

Indexed as

aldehyde dehydrogenasecardiac fibrosismyocardial infarctionWnt signaling

Identifiers

PMID26392772
PMCPMC4574798
OpenAlexW1471233511

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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.