Evidence map›Paper›PMID 31149020›Full record

ArticleNutrition & metabolism2019

High-density lipoprotein ameliorates palmitic acid-induced lipotoxicity and oxidative dysfunction in H9c2 cardiomyoblast cells via ROS suppression.

Kuen-Ming Wu, Yuan-Man Hsu, Mei-Chin Ying, Fuu-Jen Tsai, Chang-Hai Tsai, Jing-Gung Chung, Jai-Sing Yang, Chih-Hsin Tang, Li-Yi Cheng, Po-Hua Su and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

59 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  6. Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025
    Review
  7. Article
  8. Article
  9. Article
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  12. High-Density Lipoprotein and Heart Failure.Reviews in cardiovascular medicine · 2023
    Review
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  15. Article
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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 4 institutions in 2 countries.

Kuen-Ming Wu1Department of chest medicine, Jen-Ai Hospital, Taichung, Taiwan.
Yuan-Man Hsu2Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Mei-Chin Ying3Department of Food Nutrition and Health Biotechnology, Asia University, Taichung City, Taiwan.
Fuu-Jen Tsai5School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, 40402 Taiwan.
Chang-Hai Tsai6China Medical University Children's Hospital, China Medical University, Taichung, Taiwan.
Jing-Gung Chung2Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Jai-Sing YangDepartment of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan.
Chih-Hsin Tang9Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.
Li-Yi Cheng11Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Po-Hua Su12Department of Radiology, Jen-Ai Hospital, Taichung, Taiwan.
Vijaya Padma Viswanadha13Department of Biotechnology, Bharathiar University, Coimbatore, 641 046 India.
Wei-Wen Kuo *2Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Chih-Yang Huang *Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan.
China Medical University · TWChina Medical University Hospital · TWJen-Ai Hospital · TWBharathiar University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh levels circulating saturated fatty acids are associated with diabetes, obesity and hyperlipidemia. In heart, the accumulation of saturated fatty acids has been determined to play a role in the development of heart failure and diabetic cardiomyopathy. High-density lipoprotein (HDL) has been reported to possess key atheroprotective biological properties, including cellular cholesterol efflux capacity, anti-oxidative and anti-inflammatory activities. However, the underlying mechanisms are still largely unknown. Therefore, the aim of the present study is to test whether HDL could protect palmitic acid (PA)-induced cardiomyocyte injury and explore the possible mechanisms.

resultsH9c2 cells were pretreated with HDL (50-100 μg/ml) for 2 h followed by PA (0.5 mM) for indicated time period. Our results showed that HDL inhibited PA-induced cell death in a dose-dependent manner. Moreover, HDL rescued PA-induced ROS generation and the phosphorylation of JNK which in turn activated NF-κB-mediated inflammatory proteins expressions. We also found that PA impaired the balance of BCL

conclusionPA-induced ROS accumulation and results in cardiomyocyte apoptosis and inflammation. However, HDL attenuated PA-induced lipotoxicity and oxidative dysfunction via ROS suppression. These results may provide insight into a possible molecular mechanism underlying HDL suppression of the free fatty acid-induced cardiomyocyte apoptosis.

Indexed as

CardiomyoblastHigh-density lipoproteinLipotoxicityPalmitic acidROS

Identifiers

PMID31149020
PMCPMC6537189
OpenAlexW2947930584

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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.