Evidence map›Paper›PMID 38334841›Full record

ArticleJournal of cardiovascular translational research2024

Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway.

Hongjuan Cao, Lina Zhao, Yao Yuan, Chunyan Liao, Weidan Zeng, Aiyue Li, Quanfeng Huang, Yueyao Zhao, Yubing Fan, Liu Jiang and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of cardiovascular translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.1field-weighted citation impact, top 16% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  5. Metabolomic and microbial diversity perspectives onFrontiers in veterinary science · 2025
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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

13 authors at 1 institution in 1 country.

Hongjuan CaoGuizhou Medical University, Guiyang, Guizhou Province, China.
Lina ZhaoGuizhou Medical University, Guiyang, Guizhou Province, China.
Yao YuanGuizhou Medical University, Guiyang, Guizhou Province, China.
Chunyan LiaoGuizhou Medical University, Guiyang, Guizhou Province, China.
Weidan ZengGuizhou Medical University, Guiyang, Guizhou Province, China.
Aiyue LiGuizhou Medical University, Guiyang, Guizhou Province, China.
Quanfeng HuangGuizhou Medical University, Guiyang, Guizhou Province, China.
Yueyao ZhaoGuizhou Medical University, Guiyang, Guizhou Province, China.
Yubing FanGuizhou Medical University, Guiyang, Guizhou Province, China.
Liu JiangGuizhou Medical University, Guiyang, Guizhou Province, China.
Dandan SongGuizhou Medical University, Guiyang, Guizhou Province, China.
Sha LiGuizhou Medical University, Guiyang, Guizhou Province, China.
Bei ZhangGuizhou Medical University, Guiyang, Guizhou Province, China. zhangbei@gmc.edu.cn.ORCID 0000-0002-1788-6712
Guiyang Medical University · CN

Funding

National Natural Science Foundation of China No.81960315
6 · The paper itself

Abstract

The process of myocardial hypertrophy in hypertension can lead to excessive activation of oxidative stress. Lipoamide (ALM) has significant antioxidant and anti-inflammatory effects. This study aimed to investigate the effects of ALM on hypertension-induced cardiac hypertrophy, as well as explore its underlying mechanisms. We evaluated the effects of ALM on spontaneously hypertensive rats and rat cardiomyocytes treated with Ang II. We found that ALM was not effective in lowering blood pressure in SHR, but it attenuated hypertension-mediated cardiac fibrosis, oxidative stress, inflammation, and hypertrophy in rats. After that, in cultured H9C2 cells stimulated with Ang II, ALM increased the expression of antioxidant proteins that were decreased in the Ang II group. ALM also alleviated cell hypertrophy and the accumulation of ROS, while LY294002 partially abrogated these effects. Collectively, these results demonstrate that ALM could alleviate oxidative stress in cardiac hypertrophy, potentially through the activation of the PI3K/Akt-mediated Nrf2 signaling pathway.

Indexed as

CardiomegalyDisease Models, AnimalHypertensionMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRats, Inbred SHRSignal TransductionAngiotensin IIAnimalsAntihypertensive AgentsAntioxidantsBlood PressureCell LineAngiotensin IIAntihypertensive AgentsAntioxidantsNfe2l2 protein, ratNF-E2-Related Factor 2Phosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesCardiac hypertrophyLipoamideOxidative stressPI3K/Akt

Identifiers

PMID38334841
PMCPMC11371882
OpenAlexW4391692739

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.