Evidence map›Paper›PMID 27004753›Full record

ReviewBiochimica et biophysica acta2016

CD36 actions in the heart: Lipids, calcium, inflammation, repair and more?

Nada A Abumrad, Ira J Goldberg

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Endothelial Cell Regulation of Lipid Uptake During Feeding and Fasting.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  8. Article
  9. Review
  10. A CD36-based prediction model for sepsis-induced myocardial injury.International journal of cardiology. Heart & vasculature · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Observational
  19. The role of CD36 in cardiovascular disease.Cardiovascular research · 2022
    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

2 authors at 2 institutions in 1 country.

Nada A AbumradDepartments of Medicine and Cell Biology, Washington University, St. Louis, MO, United States.. Electronic address: nabumrad@wustl.edu.
Ira J GoldbergDivision of Endocrinology, Diabetes and Metabolism, New York University School of Medicine, New York, NY, United States.
New York University · USWashington University in St. Louis · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
CD36 AND INTESTINAL FAT ABSORPTIONR01DK060022 · NIDDK · WASHINGTON UNIVERSITY · PI ABUMRAD, NADA A. · 2001 to 2021
$7.7M
Pathways of Tissue Lipid UptakeR01HL045095 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABUMRAD, NADA A., GOLDBERG, IRA J · 1991 to 2024
$6.9M
FATTY ACID TRANSPORTER: REGULATION, IDENTIFICATIONR01DK033301 · NIDDK · WASHINGTON UNIVERSITY · PI ABUMRAD, NADA A. · 1986 to 2017
$5.2M
EXTRACELLULAR REGULATION OF LIPOPROTEIN LIPASE ACTIVITYR37HL045095 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA J · 2000 to 2009
$4.6M
ROLE OF CD36 IN NUTRIENT DELIVERY AND ITS DYSFUNCTION IN AFRICAN AMERICANSR01DK111175 · NIDDK · WASHINGTON UNIVERSITY · PI ABUMRAD, NADA A., ABUMRAD, NAJI N · 2016 to 2019
$1.9M
NHLBI NIH HHS R01 HL045095NHLBI NIH HHS R37 HL045095NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P30 DK056341NIDDK NIH HHS R01 DK033301NIDDK NIH HHS R01 DK060022NIDDK NIH HHS R01 DK111175
6 · The paper itself

Abstract

CD36 is a multifunctional immuno-metabolic receptor with many ligands. One of its physiological functions in the heart is the high-affinity uptake of long-chain fatty acids (FAs) from albumin and triglyceride rich lipoproteins. CD36 deletion markedly reduces myocardial FA uptake in rodents and humans. The protein is expressed on endothelial cells and cardiomyocytes and at both sites is likely to contribute to FA uptake by the myocardium. CD36 also transduces intracellular signaling events that influence how the FA is utilized and mediate metabolic effects of FA in the heart. CD36 transduced signaling regulates AMPK activation in a way that adjusts oxidation to FA uptake. It also impacts remodeling of myocardial phospholipids and eicosanoid production, effects exerted via influencing intracellular calcium (iCa(2+)) and the activation of phospholipases. Under excessive FA supply CD36 contributes to lipid accumulation, inflammation and dysfunction. However, it is also important for myocardial repair after injury via its contribution to immune cell clearance of apoptotic cells. This review describes recent progress regarding the multiple actions of CD36 in the heart and highlights those areas requiring future investigation. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk.

Indexed as

Wound HealingAnimalsCalciumCD36 AntigensHumansInflammationLipidsMyocardiumCalciumCD36 AntigensLipidsAMPKFatty acidLKB1MitochondriaSignalingUptake

Identifiers

PMID27004753
PMCPMC4983248
OpenAlexW2310847573

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.