Evidence map›Paper›PMID 30327268›Full record

ArticleEBioMedicine2018

Microtubule associated protein 4 phosphorylation leads to pathological cardiac remodeling in mice.

Lingfei Li, Qiong Zhang, Xingyue Zhang, Junhui Zhang, Xuefeng Wang, Jun Ren, Jiezhi Jia, Dongxia Zhang, Xupin Jiang, Jiaping Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. 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
2.9field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

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  20. Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Lingfei LiInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Qiong ZhangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Xingyue ZhangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Junhui ZhangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Xuefeng WangDepartment of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jun RenCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, USA.
Jiezhi JiaInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Dongxia ZhangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Xupin JiangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jiaping ZhangState Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; Department of Plastic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Hao MeiCenter for Outcomes Research and Evaluation, Yale-New Haven Hospital, CT, USA.
Bing ChenEndocrinology Department, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jiongyu HuState Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; Endocrinology Department, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address: jiongyuhu@163.com.
Yuesheng HuangInstitute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address: yshuang1958@163.com.
Southwest Hospital · CNArmy Medical University · CNUniversity of Wyoming · USYale New Haven Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac remodeling is a pathophysiological process that involves various changes in heart, including cardiac hypertrophy and fibrosis. Cardiac remodeling following pathological stimuli is common trigger leading to cardiac maladaptation and onset of heart failure, and their pathogenesis remains unclear.

methodsHeart specimens of tetralogy of Fallot (TOF) patients, myocardial infarction (MI) and transverse aortic constriction (TAC) mouse models were collected to determine changes of microtubule associated protein 4 (MAP4) phosphorylation. MAP4 (S667A, S737E and S760E) knock in (MAP4 KI) mouse and cultured neonatal mouse cardiomyocytes or fibroblasts were used to investigate changes of cardiac phenotypes and possible mechanisms with a variety of approaches, including functional, histocytological and pathological observations.

findingsElevated cardiac phosphorylation of MAP4 (S737 and S760) was observed in TOF patients, MI and TAC mouse models. In MAP4 KI mice, age-dependent cardiac phenotypes, including cardiac hypertrophy, fibrosis, diastolic and systolic dysfunction were observed. In addition, increased cardiomyocyte apoptosis together with microtubule disassembly and mitochondrial translocation of phosphorylated MAP4 was detected prior to the onset of cardiac remodeling, and p38/MAPK was demonstrated to be the possible signaling pathway that mediated MAP4 (S737 and S760) phosphorylation.

interpretationOur data reveal for the first time that MAP4 drives pathological cardiac remodeling through its phosphorylation. These findings bear the therapeutic potential to ameliorate pathological cardiac remodeling by attenuating MAP4 phosphorylation. FUND: This work was supported by the Key Program of National Natural Science Foundation of China (No.81430042) and National Natural Science Foundation of China (No.81671913).

Indexed as

AnimalsAortic DiseasesDisease Models, AnimalFemaleFibroblastsHumansMaleMiceMice, TransgenicMicrotubule-Associated ProteinsMutation, MissenseMyocytes, CardiacPhosphorylationTetralogy of FallotMicrotubule-Associated ProteinsApoptosisCardiac remodelingMAP4MicrotubuleMitochondria

Identifiers

PMID30327268
PMCPMC6286641
OpenAlexW2896253748

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.