Evidence map›Paper›PMID 30373812›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

microRNA-378 promotes autophagy and inhibits apoptosis in skeletal muscle.

Yan Li, Jingjing Jiang, Wei Liu, Hui Wang, Lei Zhao, Shengnan Liu, Peng Li, Shengjie Zhang, Chao Sun, Yuting Wu and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
8.3field-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

79 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. [Advances in the role of miR-378a in skeletal muscle development and diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. miR-378a-5p targeting BRAF regulates CD4Frontiers in immunology · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Acta biochimica et biophysica Sinica · 2024
    Article
  18. Review
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

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

20 authors at 7 institutions in 2 countries.

Yan LiState Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 214122 Wuxi, China.
Jingjing JiangDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Wei LiuChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Hui WangChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Lei ZhaoDepartment of Neuromuscular Disease, Children's Hospital of Fudan University, 201102 Shanghai, China.
Shengnan LiuChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Peng LiChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Shengjie ZhangChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Chao SunChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Yuting WuChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Shuxian YuChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Xihua LiDepartment of Neuromuscular Disease, Children's Hospital of Fudan University, 201102 Shanghai, China.
Hui ZhangState Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 214122 Wuxi, China.
Haifeng QianState Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 214122 Wuxi, China.
Duo ZhangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University Medical Campus, Boston, MA 02118.
Feifan GuoChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Qiwei ZhaiChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Qiurong DingChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China.
Li WangState Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 214122 Wuxi, China; wangli@jiangnan.edu.cn yinghao@sibs.ac.cn.
Hao YingChinese Academy of Sciences Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China; wangli@jiangnan.edu.cn yinghao@sibs.ac.cn.
Shanghai Institutes for Biological Sciences · CNChinese Academy of Sciences · CNChildren's Hospital of Fudan University · CNState Key Laboratory of Food Science and Technology · CNBoston Medical Center · USJiangnan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabolic regulation of cell death is sophisticated. A growing body of evidence suggests the existence of multiple metabolic checkpoints that dictate cell fate in response to metabolic fluctuations. However, whether microRNAs (miRNAs) are able to respond to metabolic stress, reset the threshold of cell death, and attempt to reestablish homeostasis is largely unknown. Here, we show that miR-378/378* KO mice cannot maintain normal muscle weight and have poor running performance, which is accompanied by impaired autophagy, accumulation of abnormal mitochondria, and excessive apoptosis in skeletal muscle, whereas miR-378 overexpression is able to enhance autophagy and repress apoptosis in skeletal muscle of mice. Our in vitro data show that metabolic stress-responsive miR-378 promotes autophagy and inhibits apoptosis in a cell-autonomous manner. Mechanistically, miR-378 promotes autophagy initiation through the mammalian target of rapamycin (mTOR)/unc-51-like autophagy activating kinase 1 (ULK1) pathway and sustains autophagy via Forkhead box class O (FoxO)-mediated transcriptional reinforcement by targeting phosphoinositide-dependent protein kinase 1 (PDK1). Meanwhile, miR-378 suppresses intrinsic apoptosis initiation directly through targeting an initiator caspase-Caspase 9. Thus, we propose that miR-378 is a critical component of metabolic checkpoints, which integrates metabolic information into an adaptive response to reduce the propensity of myocytes to undergo apoptosis by enhancing the autophagic process and blocking apoptotic initiation. Lastly, our data suggest that inflammation-induced down-regulation of miR-378 might contribute to the pathogenesis of muscle dystrophy.

Indexed as

3-Phosphoinositide-Dependent Protein KinasesAnimalsApoptosisAutophagyAutophagy-Related Protein-1 HomologCaspase 9Forkhead Box Protein O1MaleMiceMice, KnockoutMicroRNAsMuscle CellsMuscle, SkeletalRunningSignal TransductionStress, Physiological3-Phosphoinositide-Dependent Protein KinasesAutophagy-Related Protein-1 HomologCasp9 protein, mouseCaspase 9Forkhead Box Protein O1Foxo1 protein, mouseMicroRNAsMIRN378 microRNA, mousePdpk1 protein, mouseTOR Serine-Threonine KinasesUlk1 protein, mouseapoptosisautophagymiR-378skeletal muscle

Identifiers

PMID30373812
PMCPMC6243236
OpenAlexW2899153893

What OpenQuestion holds

Textmetadata
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.