Evidence map›Paper›PMID 24820416›Full record

ArticleMolecular and cellular biology2014

Deficiency of a lipid droplet protein, perilipin 5, suppresses myocardial lipid accumulation, thereby preventing type 1 diabetes-induced heart malfunction.

Kenta Kuramoto, Fumie Sakai, Nana Yoshinori, Tomoe Y Nakamura, Shigeo Wakabayashi, Tomoko Kojidani, Tokuko Haraguchi, Fumiko Hirose, Takashi Osumi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Perilipins at a glance.Journal of cell science · 2022
    Article
  12. Plin5 Bidirectionally Regulates Lipid Metabolism in Oxidative Tissues.Oxidative medicine and cellular longevity · 2022
    Review
  13. Plin5, a New Target in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors at 4 institutions in 1 country.

Kenta Kuramoto
Fumie Sakai
Nana Yoshinori
Tomoe Y Nakamura
Shigeo Wakabayashi
Tomoko Kojidani
Tokuko Haraguchi
Fumiko Hirose
Takashi Osumi
University of Hyogo · JPNational Cerebral and Cardiovascular Center · JPJapan Women's University · JPNational Institute of Information and Communications Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid droplet (LD) is a ubiquitous organelle that stores triacylglycerol and other neutral lipids. Perilipin 5 (Plin5), a member of the perilipin protein family that is abundantly expressed in the heart, is essential to protect LDs from attack by lipases, including adipose triglyceride lipase. Plin5 controls heart metabolism and performance by maintaining LDs under physiological conditions. Aberrant lipid accumulation in the heart leads to organ malfunction, or cardiomyopathy. To elucidate the role of Plin5 in a metabolically disordered state and the mechanism of lipid-induced cardiomyopathy, we studied the effects of streptozotocin-induced type 1 diabetes in Plin5-knockout (KO) mice. In contrast to diabetic wild-type mice, diabetic Plin5-KO mice lacked detectable LDs in the heart and did not exhibit aberrant lipid accumulation, excessive reactive oxygen species (ROS) generation, or heart malfunction. Moreover, diabetic Plin5-KO mice exhibited lower heart levels of lipotoxic molecules, such as diacylglycerol and ceramide, than wild-type mice. Membrane translocation of protein kinase C and the assembly of NADPH oxidase 2 complex on the membrane were also suppressed. The results suggest that diabetic Plin5-KO mice are resistant to type 1 diabetes-induced heart malfunction due to the suppression of the diacylglycerol/ceramide-protein kinase C pathway and of excessive ROS generation by NADPH oxidase.

Indexed as

AnimalsCardiomyopathiesCeramidesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1DiglyceridesLipid DropletsMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMyocardiumNADPH Oxidase 2NADPH OxidasesPerilipin-5Protein Kinase CCeramidesCybb protein, mouseDiglyceridesMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesPerilipin-5Plin5 protein, mouseProtein Kinase CProteinsReactive Oxygen SpeciesStreptozocinTriglycerides

Identifiers

PMID24820416
PMCPMC4097652
OpenAlexW2133818377

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.