Evidence map›Paper›PMID 30028636›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Loss of lipin 1-mediated phosphatidic acid phosphohydrolase activity in muscle leads to skeletal myopathy in mice.

George G Schweitzer, Sara L Collier, Zhouji Chen, Kyle S McCommis, Sara K Pittman, Jun Yoshino, Scot J Matkovich, Fong-Fu Hsu, Roman Chrast, James M Eaton and 3 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Role of lipins in cardiovascular diseases.Lipids in health and disease · 2023
    Review
  11. Article
  12. Article
  13. Low lysophosphatidylcholine induces skeletal muscle myopathy that is aggravated by high-fat diet feeding.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  14. Article
  15. Article
  16. Metabolic Alterations in Myotonic Dystrophy Type 1 and Their Correlation with Lipin.International journal of environmental research and public health · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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 at 3 institutions in 2 countries.

George G SchweitzerDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Sara L CollierDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Zhouji ChenDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Kyle S McCommisDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Sara K PittmanDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Jun YoshinoDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Scot J MatkovichCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Fong-Fu HsuDivision of Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Roman ChrastDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden; and.
James M EatonDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia, USA.
Thurl E HarrisDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia, USA.
Conrad C WeihlDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Brian N FinckDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Washington University in St. Louis · USUniversity of Virginia · USKarolinska Institutet · SE

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Clay F. Semenkovich · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
DIABETES &RELATED METABOLIC DISEASEST32DK007120 · NIDDK · WASHINGTON UNIVERSITY · PI MARCO COLONNA, Maria Sara Remedi · 1986 to 2026
$15.7M
Washington University Institute of Clinical and Translational Sciences (KL2) KL2TR002346 · NCATS · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 2017 to 2026
$14.0M
TrainingP41GM103422 · NIGMS · WASHINGTON UNIVERSITY · PI YARASHESKI, KEVIN E · 2012 to 2019
$12.0M
PRINCIPLES IN CARDIVASCULAR RESEARCH TRAINING PROGRAMT32HL007081 · NHLBI · WASHINGTON UNIVERSITY · PI Abhinav Diwan, Karen Ellen Joynt Maddox · 1985 to 2026
$10.6M
VCP in myopathy and dementiaR01AG031867 · NIA · WASHINGTON UNIVERSITY · PI CONRAD C WEIHL · 2009 to 2026
$9.1M
Washington University Institute of Clinical and Translational SciencesKL2TR000450 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$8.8M
NCATS NIH HHS KL2 TR000450NCATS NIH HHS KL2 TR002346NCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1 TR002345NCI NIH HHS P30 CA091842NHLBI NIH HHS R01 HL119225NHLBI NIH HHS T32 HL007081NHLBI NIH HHS T32 HL007275NIAMS NIH HHS K24 AR073317NIAMS NIH HHS R01 AR068797NIA NIH HHS R01 AG031867NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P60 DK020579NIDDK NIH HHS R01 DK078187NIDDK NIH HHS R01 DK101946NIDDK NIH HHS R01 DK104995NIDDK NIH HHS T32 DK007120NIGMS NIH HHS P41 GM103422NIGMS NIH HHS T32 GM007055
6 · The paper itself

Abstract

Lipin 1 regulates glycerolipid homeostasis by acting as a phosphatidic acid phosphohydrolase (PAP) enzyme in the triglyceride-synthesis pathway and by regulating transcription factor activity. Mutations in human lipin 1 are a common cause of recurrent rhabdomyolysis in children. Mice with constitutive whole-body lipin 1 deficiency have been used to examine mechanisms connecting lipin 1 deficiency to myocyte injury. However, that mouse model is confounded by lipodystrophy not phenocopied in people. Herein, 2 muscle-specific mouse models were studied: 1) Lpin1 exon 3 and 4 deletion, resulting in a hypomorphic protein without PAP activity, but which preserved transcriptional coregulatory function; and 2) Lpin1 exon 7 deletion, resulting in total protein loss. In both models, skeletal muscles exhibited a chronic myopathy with ongoing muscle fiber necrosis and regeneration and accumulation of phosphatidic acid and, paradoxically, diacylglycerol. Additionally, lipin 1-deficient mice had abundant, but abnormal, mitochondria likely because of impaired autophagy. Finally, these mice exhibited increased plasma creatine kinase following exhaustive exercise when unfed. These data suggest that mice lacking lipin 1-mediated PAP activity in skeletal muscle may serve as a model for determining the mechanisms by which lipin 1 deficiency leads to myocyte injury and for testing potential therapeutic approaches.-Schweitzer, G. G., Collier, S. L., Chen, Z., McCommis, K. S., Pittman, S. K., Yoshino, J., Matkovich, S. J., Hsu, F.-F., Chrast, R., Eaton, J. M., Harris, T. E., Weihl, C. C., Finck, B. N. Loss of lipin 1-mediated phosphatidic acid phosphohydrolase activity in muscle leads to skeletal myopathy in mice.

Indexed as

Disease Models, AnimalGene Expression RegulationAnimalsAutophagyFemaleGene Expression ProfilingMiceMice, Inbred C57BLMuscle, SkeletalMuscular DiseasesNuclear ProteinsPhosphatidate PhosphatasePhosphatidic AcidsLpin1 protein, mouseNuclear ProteinsPhosphatidate PhosphatasePhosphatidic AcidsautophagydiacylglycerolLPIN1rhabdomyolysistriacylglycerol

Identifiers

PMID30028636
PMCPMC6355067
OpenAlexW2883485637

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.