Evidence map›Paper›PMID 24895128›Full record

ArticleThe Journal of biological chemistry2014

Mitochondrial complex I deficiency enhances skeletal myogenesis but impairs insulin signaling through SIRT1 inactivation.

Jin Hong, Bong-Woo Kim, Hyo-Jung Choo, Jung-Jin Park, Jae-Sung Yi, Dong-Min Yu, Hyun Lee, Gye-Soon Yoon, Jae-Seon Lee, Young-Gyu Ko

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  4. American journal of physiology. Cell physiology · 2025
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  6. High-fat diet during pregnancy promotes fetal skeletal muscle fatty acid oxidation and insulin resistance in an ovine model.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
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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

10 authors at 2 institutions in 1 country.

Jin HongFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Bong-Woo KimDepartment of Cosmetic Science and Technology, Seowon University, Cheongju, 361-742, Korea.
Hyo-Jung ChooFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Jung-Jin ParkFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Jae-Sung YiFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Dong-Min YuFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Hyun LeeFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea.
Gye-Soon YoonDepartment of Biochemistry and Molecular Biology, Ajou University, Suwon 443-721, Korea, and.
Jae-Seon LeeDepartment of Biomedical Sciences, College of Medicine, Inha University, Incheon, 400-712, Korea.
Young-Gyu KoFrom the Division of Life Sciences, Korea University, Seoul, 136-701, Korea, ygko@korea.ac.kr.
Inha University · KRSeowon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To address whether mitochondrial biogenesis is essential for skeletal myogenesis, C2C12 myogenesis was investigated after knockdown of NADH dehydrogenase (ubiquintone) flavoprotein 1 (NDUFV1), which is an oxidative phosphorylation complex I subunit that is the first subunit to accept electrons from NADH. The NDUFVI knockdown enhanced C2C12 myogenesis by decreasing the NAD(+)/NADH ratio and subsequently inactivating SIRT1 and SIRT1 activators (pyruvate, SRT1720, and resveratrol) abolished the NDUFV1 knockdown-induced myogenesis enhancement. However, the insulin-elicited activation of insulin receptor β (IRβ) and insulin receptor substrate-1 (IRS-1) was reduced with elevated levels of protein-tyrosine phosphatase 1B after NDUFV1 knockdown in C2C12 myotubes. The NDUFV1 knockdown-induced blockage of insulin signaling was released by protein-tyrosine phosphatase 1B knockdown in C2C12 myotubes, and we found that NDUFV1 or SIRT1 knockdown did not affect mitochondria biogenesis during C2C12 myogenesis. Based on these data, we can conclude that complex I dysfunction-induced SIRT1 inactivation leads to myogenesis enhancement but blocks insulin signaling without affecting mitochondria biogenesis.

Indexed as

AnimalsCell LineElectron Transport Complex IGene Knockdown TechniquesInsulinInsulin ResistanceMiceMitochondrial DiseasesModels, BiologicalMuscle DevelopmentMuscle Fibers, SkeletalMuscle, SkeletalNADOxidative PhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 1RNA, Small InterferingElectron Transport Complex IInsulinNADNDUFV1 protein, mouseProtein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, mouseRNA, Small InterferingSirt1 protein, mouseSirtuin 1Insulin ResistanceMitochondrial DiseaseMitochondrial MetabolismMyogenesisSirtuin 1 (SIRT1)

Identifiers

PMID24895128
PMCPMC4106319
OpenAlexW2024322480

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.