Evidence map›Paper›PMID 27506764›Full record

ArticleEMBO molecular medicine2016

Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit.

Jing Liu, Xijun Liang, Danxia Zhou, Ling Lai, Liwei Xiao, Lin Liu, Tingting Fu, Yan Kong, Qian Zhou, Rick B Vega and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Review
  9. Mitochondrial proteostasis regulated by CRL5Communications biology · 2025
    Article
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14 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

14 authors at 3 institutions in 2 countries.

Jing LiuState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Xijun LiangState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Danxia ZhouState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Ling LaiDiabetes and Obesity Research Center, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, USA.
Liwei XiaoState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Lin LiuState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Tingting FuState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Yan KongDepartment of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, China.
Qian ZhouState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Rick B VegaDiabetes and Obesity Research Center, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, USA.
Min-Sheng ZhuState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Daniel P KellyDiabetes and Obesity Research Center, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, USA.
Xiang GaoState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
Zhenji GanState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China ganzj@nju.edu.cn.ORCID 0000-0001-5940-207X
Model Animal Research Center · CNSanford Burnham Prebys Medical Discovery Institute · USSoutheast University · CN

Funding

REGULATION OF FATTY ACID OXIDATION DURING CARDIAC GROWTHR01HL058493 · NHLBI · WASHINGTON UNIVERSITY · PI KELLY, DANIEL PATRICK · 1998 to 2024
$10.6M
Molecular Control of Muscle Fuel MetabolismR01DK045416 · NIDDK · WASHINGTON UNIVERSITY · PI KELLY, DANIEL PATRICK · 1996 to 2020
$8.1M
NHLBI NIH HHS R01 HL058493NIDDK NIH HHS R01 DK045416
6 · The paper itself

Abstract

Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative-type fibers. However, the mechanism for coupling of mitochondrial function to the muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR-208b/miR-499, parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1α-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, an AMP-activated protein kinase (AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1α. Inhibition of Fnip1 reactivated AMPK/PGC-1α signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD Thus, we have identified a miR-499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function.

Indexed as

Adaptation, PhysiologicalGene Expression RegulationAMP-Activated Protein KinasesAnimalsCarrier ProteinsMice, Inbred C57BLMice, Inbred mdxMice, KnockoutMicroRNAsMitochondriaMuscle Fibers, SkeletalMyosin Heavy ChainsMyosin Type IIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSignal TransductionAMP-Activated Protein KinasesCarrier ProteinsFNIP1 protein, mouseMicroRNAsMirn208 microRNA, mouseMIRN499 microRNA, mouseMyh14 protein, mouseMyh7 protein, mouseMyosin Heavy ChainsMyosin Type IIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mousecontractile fiber typegene regulationmicroRNAmitochondrial functionmuscle

Identifiers

PMID27506764
PMCPMC5048369
OpenAlexW2511737947

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.