Evidence mapPaperPMID 38422177Full record

ArticleCirculation research2024

Glycolysis-Mediated Activation of v-ATPase by Nicotinamide Mononucleotide Ameliorates Lipid-Induced Cardiomyopathy by Repressing the CD36-TLR4 Axis.

Shujin Wang, Yinying Han, Ruimin Liu, Mengqian Hou, Dietbert Neumann, Jun Zhang, Fang Wang, Yumeng Li, Xueya Zhao, Francesco Schianchi and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Circulation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 11 institutions in 3 countries.

Shujin Wang *Institute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).ORCID 0009-0000-2278-8271
Yinying Han *Institute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).ORCID 0009-0006-4641-047X
Ruimin Liu *Institute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).ORCID 0009-0009-2013-9601
Mengqian Hou *Institute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).
Dietbert NeumannDepartment of Pathology (D.N.), Maastricht University Medical Center+, the Netherlands.ORCID 0000-0002-4316-684X
Jun ZhangInstitute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).ORCID 0000-0002-5843-8705
Fang WangDepartment of Genetics and Cell Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, the Netherlands (S.W., F.W., F.S., M.N., J.F.C.G., J.J.F.P.L.).
Yumeng LiTianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences, China (Y.L., X.W.).ORCID 0000-0002-9986-5201
Xueya ZhaoInstitute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).
Francesco SchianchiDepartment of Genetics and Cell Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, the Netherlands (S.W., F.W., F.S., M.N., J.F.C.G., J.J.F.P.L.).ORCID 0000-0002-9385-910X
Chao DaiCAS Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences (CAS), Changsha, China (C.D., X.W.).ORCID 0009-0007-0701-0059
Lizhong LiuDepartment of Physiology, Shenzhen University Medical School, Shenzhen University, China (L.L.).ORCID 0000-0003-4751-1679
Miranda NabbenDepartment of Genetics and Cell Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, the Netherlands (S.W., F.W., F.S., M.N., J.F.C.G., J.J.F.P.L.).ORCID 0000-0002-5691-1634
Jan F C GlatzDepartment of Genetics and Cell Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, the Netherlands (S.W., F.W., F.S., M.N., J.F.C.G., J.J.F.P.L.).ORCID 0000-0001-6533-9548
Xin WuCAS Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences (CAS), Changsha, China (C.D., X.W.).ORCID 0000-0002-9225-5574
Xifeng LuClinical Research Center, First Affiliated Hospital of Shantou University Medical College, China (X. Lu).ORCID 0000-0002-4782-0300
Xi LiInstitute of Life Sciences, School of Basic Medicine, Chongqing Medical University, China (S.W., Y.H., R.L., M.H., J.Z., X.Z., X. Li).
Joost J F P LuikenDepartment of Genetics and Cell Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, the Netherlands (S.W., F.W., F.S., M.N., J.F.C.G., J.J.F.P.L.).ORCID 0000-0002-8808-2631
Maastricht University · NLChongqing Medical University · CNInstitute of Subtropical Agriculture · CNAnhui Medical University · CNBeijing Anzhen Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNMaastricht School of Management · NLMaastricht University Medical Centre · NLShantou University · CNShenzhen University · CNTianjin Institute of Industrial Biotechnology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic overconsumption of lipids followed by their excessive accumulation in the heart leads to cardiomyopathy. The cause of lipid-induced cardiomyopathy involves a pivotal role for the proton-pump vacuolar-type H

methodsRats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly). We used the following methods: RNA sequencing, mRNA/protein expression analysis, immunofluorescence microscopy, (co)immunoprecipitation/proximity ligation assay (v-ATPase assembly), myocellular uptake of [

resultsNMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance. Lipidomics revealed C18:1-enriched diacylglycerols as lipid class prominently increased by high-fat diet and subsequently reversed/preserved by lysine/leucine/arginine/NMN treatment. Studies with mTORC1/v-ATPase inhibitors and heart-specific v-ATPase-knockout mice further confirmed the pivotal roles of v-ATPase in these beneficial actions.

conclusionNMN preserves heart function during lipid overload by preventing v-ATPase disassembly.

Indexed as

CardiomyopathiesInsulin ResistanceAdenosine TriphosphatasesAnimalsArginineCD36 AntigensFibrosisInflammationLeucineLipidsLysineMechanistic Target of Rapamycin Complex 1MiceMyocytes, CardiacNicotinamide MononucleotideRatsAdenosine TriphosphatasesArginineAtp6v0d2 protein, mouseCD36 AntigensCd36 protein, mouseLeucineLipidsLysineMechanistic Target of Rapamycin Complex 1Nicotinamide MononucleotideTlr4 protein, mouseToll-Like Receptor 4Vacuolar Proton-Translocating ATPasesdiabetic cardiomyopathiesendosomesfibrosisinsulin resistancelipid metabolismtoll-like receptor 4

Identifiers

PMID38422177
PMCPMC10906217
OpenAlexW4391612709

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.