Evidence map›Paper›PMID 31199069›Full record

ArticleJournal of cellular and molecular medicine2019

4-O-methylhonokiol protects against diabetic cardiomyopathy in type 2 diabetic mice by activation of AMPK-mediated cardiac lipid metabolism improvement.

Zongyu Zheng, Tianjiao Ma, Hua Guo, Ki Soo Kim, Kyoung Tae Kim, Liqi Bi, Zhiguo Zhang, Lu Cai

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The Active Ingredient Catalpol inDiabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. 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

8 authors at 5 institutions in 2 countries.

Zongyu ZhengDepartments of Urology and Cardiology, The First Hospital of Jilin University, Changchun, China.
Tianjiao MaDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, Kentucky.
Hua GuoDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, Kentucky.
Ki Soo KimSK Bioland Haimen Co. LTD, Haimen, China.
Kyoung Tae KimSK Bioland Haimen Co. LTD, Haimen, China.
Liqi BiDepartment of Rheumatology and Immunology, China-Japan Union Hospital of Jilin University, Changchun, China.
Zhiguo ZhangDepartments of Urology and Cardiology, The First Hospital of Jilin University, Changchun, China.
Lu CaiDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, Kentucky.ORCID 0000-0003-3048-1135
Haier Group (China) · CNUnion Hospital · CNUniversity of Louisville · USJilin University · CNNingbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy (DCM) is characterized by increased left ventricular mass and wall thickness, decreased systolic function, reduced ejection fraction (EF) and ultimately heart failure. The 4-O-methylhonokiol (MH) has been isolated mainly from the bark of the root and stem of Magnolia species. In this study, we aimed to elucidate whether MH can effectively prevent DCM in type 2 diabetic (T2D) mice and, if so, whether the protective response of MH is associated with its activation of AMPK-mediated inhibition of lipid accumulation and inflammation. A total number of 40 mice were divided into four groups: Ctrl, Ctrl + MH, T2D, T2D + MH. Five mice from each group were sacrificed after 3-month MH treatment. The remaining animals in each group were kept for additional 3 months without further MH treatment. In T2D mice, the typical DCM symptoms were induced as expected, reflected by decreased ejection fraction and lipotoxic effects inducing lipid accumulation, oxidative stress, inflammatory reactions, and final fibrosis. However, these typical DCM changes were significantly prevented by the MH treatment immediately or 3 months after the 3-month MH treatment, suggesting MH-induced cardiac protection from T2D had a memory effect. Mechanistically, MH cardiac protection from DCM may be associated with its lipid metabolism improvement by the activation of AMPK/CPT1-mediated fatty acid oxidation. In addition, the MH treatment of DCM mice significantly improved their insulin resistance levels by activation of GSK-3β. These results indicate that the treatment of T2D with MH effectively prevents DCM probably via AMPK-dependent improvement of the lipid metabolism.

Indexed as

Lipid MetabolismAMP-Activated Protein KinasesAnimalsBiphenyl CompoundsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic CardiomyopathiesFibrosisInflammationLignansMaleMice, Inbred C57BLModels, BiologicalOxidative Stress4-O-methylhonokiolAMP-Activated Protein KinasesBiphenyl CompoundsBlood GlucoseLignans4-O-methylhonokiolAMPKdiabetic cardiomyopathy

Identifiers

PMID31199069
PMCPMC6653553
OpenAlexW2949564246

What OpenQuestion holds

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LicenceCC BY
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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.