Evidence map›Paper›PMID 38753506›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Deletion of TECRL promotes skeletal muscle repair by up-regulating EGR2.

Sha Geng, Song-Bai Liu, Wei He, Xiangbin Pan, Yi Sun, Ting Xue, Shiyuan Han, Jing Lou, Ying Chang, Jiqing Zheng and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. 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
–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

11 citing papers in PubMed.

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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.

Sha Geng *Cyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.ORCID 0009-0007-7833-1351
Song-Bai Liu *Suzhou Key Laboratory of Medical Biotechnology, Suzhou Vocational Health College, Suzhou 215009, People's Republic of China.ORCID 0000-0002-3920-1032
Wei He *Cyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.ORCID 0000-0003-4793-7792
Xiangbin Pan *Department of Structural Heart Disease, National Center for Cardiovascular Disease, China and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Yi Sun *Department of Cardiovascular Surgery, Fuwai Yunnan Cardiovascular Hospital, Kunming 650102, People's Republic of China.ORCID 0000-0003-2984-1957
Ting XueCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.
Shiyuan HanCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.ORCID 0009-0006-5769-6020
Jing LouCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.
Ying ChangCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.ORCID 0009-0008-9146-8122
Jiqing ZhengCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.
Xinghong ShiCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.ORCID 0009-0002-8903-8867
Yangxin LiDepartment of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou Jiangsu 215000, People's Republic of China.
Yao-Hua SongCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215123, People's Republic of China.

Funding

National Natural Science Foundation of ChinaThe project for the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)The Project of State Key Laboratory of Radiation Medicine and Protection, Soochow University
6 · The paper itself

Abstract

Myogenic regeneration relies on the proliferation and differentiation of satellite cells. TECRL (trans-2,3-enoyl-CoA reductase like) is an endoplasmic reticulum protein only expressed in cardiac and skeletal muscle. However, its role in myogenesis remains unknown. We show that TECRL expression is increased in response to injury. Satellite cell-specific deletion of TECRL enhances muscle repair by increasing the expression of EGR2 through the activation of the ERK1/2 signaling pathway, which in turn promotes the expression of PAX7. We further show that TECRL deletion led to the upregulation of the histone acetyltransferase general control nonderepressible 5, which enhances the transcription of EGR2 through acetylation. Importantly, we showed that AAV9-mediated TECRL silencing improved muscle repair in mice. These findings shed light on myogenic regeneration and muscle repair.

Indexed as

Early Growth Response Protein 2Muscle DevelopmentMuscle, SkeletalRegenerationAnimalsCell DifferentiationMAP Kinase Signaling SystemMiceMice, KnockoutPAX7 Transcription FactorSatellite Cells, Skeletal MuscleUp-RegulationEarly Growth Response Protein 2Egr2 protein, mousePax7 protein, mousePAX7 Transcription Factorischemiamuscle regenerationsatellite cell

Identifiers

PMID38753506
PMCPMC11126978

What OpenQuestion 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 OpenQuestion graph.