Evidence map›Paper›PMID 21851295›Full record

ReviewCritical reviews in biochemistry and molecular biology2011

Lipotoxicity and cardiac dysfunction in mammals and Drosophila.

Ryan Tyge Birse, Rolf Bodmer

Abstract readReview
In one paragraph

Review in Critical reviews in biochemistry and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Lipotoxicity, ER Stress, and Cardiovascular Disease: Current Understanding and Future Directions.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Tissue-specific analysis of lipid species inJournal of lipid research · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Journal of cardiovascular development and disease · 2016
    Review
  14. Gaining Insights into Diabetic Cardiomyopathy from Drosophila.Trends in endocrinology and metabolism: TEM · 2015
    Review
  15. Article
  16. Obesity-associated cardiac dysfunction in starvation-selected Drosophila melanogaster.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Article
  17. Article
  18. Methods for studying metabolism in Drosophila.Methods (San Diego, Calif.) · 2014
    Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Ryan Tyge BirseDevelopment and Aging Program, Sanford-Burnham Medical Research Institute , La Jolla, CA , USA.
Rolf Bodmer
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

HEART DEVELOPMENT IN DROSOPHILAR01HL054732 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BODMER, ROLF · 1995 to 2024
$11.3M
Systems Biology CoreP01HL098053 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HADDAD, GABRIEL G · 2010 to 2014
$10.2M
GENETIC ANALYSIS OF SLEEP SENECENCEP01AG033561 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI BODMER, ROLF · 2011 to 2015
$6.3M
Probing the adipocyte-myocyte axis: An Interdisciplinary ApproachR24DK084969 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI BODMER, ROLF, GULICK, TOD · 2010 to 2010
$573k
NHLBI NIH HHS P01 HL098053NHLBI NIH HHS R01 HL054732NIA NIH HHS P01 AG033561NIDDK NIH HHS R24 DK084969
6 · The paper itself

Abstract

The lipotoxic effects of obesity are important contributing factors in cancer, diabetes, and cardiovascular disease (CVD), but the genetic mechanisms, by which lipotoxicity influences the initiation and progression of CVD are poorly understood. Hearts, of obese and diabetic individuals, exhibit several phenotypes in common, including ventricular remodeling, prolonged QT intervals, enhanced frequency of diastolic and/or systolic dysfunction, and decreased fractional shortening. High systemic lipid concentrations are thought to be the leading cause of lipid-related CVD in obese or diabetic individuals. However, an alternative possibility is that obesity leads to cardiac-specific steatosis, in which lipids and their metabolites accumulate within the myocardial cells themselves and thereby disrupt normal cardiovascular function. Drosophila has recently emerged as an excellent model to study the fundamental genetic mechanisms of metabolic control, as well as their relationship to heart function. Two recent studies of genetic and diet-induced cardiac lipotoxicity illustrate this. One study found that alterations in genes associated with membrane phospholipid metabolism may play a role in the abnormal lipid accumulation associated with cardiomyopathies. The second study showed that Drosophila fed a diet high in saturated fats, developed obesity, dysregulated insulin and glucose homeostasis, and severe cardiac dysfunction. Here, we review the current understanding of the mechanisms that contribute to the detrimental effects of dysregulated lipid metabolism on cardiovascular function. We also discuss how the Drosophila model could help elucidate the basic genetic mechanisms of lipotoxicity- and metabolic syndrome-related cardiomyopathies in mammals.

Indexed as

Disease Models, AnimalLipid MetabolismAnimalsCardiovascular DiseasesDiabetes ComplicationsDrosophilaGlucoseHumansInsulinMetabolic SyndromeObesityPhospholipidsGlucoseInsulinPhospholipids

Identifiers

PMID21851295
PMCPMC4386717
OpenAlexW2007258443

What OpenQuestion holds

Textmetadata
LicenceTDM
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.