Evidence map›Paper›PMID 38837607›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Targeting Rab7-Rilp Mediated Microlipophagy Alleviates Lipid Toxicity in Diabetic Cardiomyopathy.

Jiahan Ke, Jianan Pan, Hao Lin, Shuying Huang, Junfeng Zhang, Changqian Wang, Alex Chia Yu Chang, Jun Gu

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Review
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  4. Observational
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  16. Guidelines for diet-induced models of cardiometabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  17. 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.

Jiahan KeDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Jianan PanDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Hao LinDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Shuying HuangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Junfeng ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Changqian WangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Alex Chia Yu ChangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.
Jun GuDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200001, China.ORCID 0000-0002-1847-7304

Funding

National Natural Science Foundation of China #81670293National Natural Science Foundation of China #82070381National Natural Science Foundation of China #82270356Shanghai Science and Technology Commission #20ZR1431100Shanghai Science and Technology Commission #23ZR1437200
6 · The paper itself

Abstract

Diabetic cardiomyopathy (DbCM) is characterized by diastolic dysfunction, which progresses into heart failure and aberrant electrophysiology in diabetic patients. Dyslipidemia in type 2 diabetic patients leads to the accumulation of lipid droplets (LDs) in cardiomyocytes and results in lipid toxicity which has been suggested to drive DbCM. It is aimed to explore potential pathways that may boost LDs degradation in DbCM and restore cardiac function. LDs accumulation resulted in an increase in lipid toxicity in DbCM hearts is confirmed. Microlipophagy pathway, rather than traditional macrolipophagy, is activated in DbCM hearts. RNA-Seq data and Rab7-CKO mice implicate that Rab7 is a major modulator of the microlipophagy pathway. Mechanistically, Rab7 is phosphorylated at Tyrosine 183, which allows the recruitment of Rab-interacting lysosome protein (Rilp) to proceed LDs degradation by lysosome. Treating DbCM mice with Rab7 activator ML-098 enhanced Rilp level and rescued the observed cardiac dysfunction. Overall, Rab7-Rilp-mediated microlipophagy may be a promising target in the treatment of lipid toxicity in DbCM is suggested.

Indexed as

Diabetic Cardiomyopathiesrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsAdaptor Proteins, Signal TransducingAnimalsAutophagyDisease Models, AnimalLipid DropletsLipid MetabolismMaleMiceMice, KnockoutMyocytes, CardiacAdaptor Proteins, Signal Transducingrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, mouserab GTP-Binding ProteinsRilp protein, mousediabetic cardiomyopathylipid toxicitylipophagy

Identifiers

PMID38837607
PMCPMC11304244

What OpenQuestion holds

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Registered trials

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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.