Evidence map›Paper›PMID 21070851›Full record

ArticleFree radical biology & medicine2011

Fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury.

Partha Mukhopadhyay, Bėla Horváth, Mohanraj Rajesh, Shingo Matsumoto, Keita Saito, Sándor Bátkai, Vivek Patel, Galin Tanchian, Rachel Y Gao, Benjamin F Cravatt and 2 more

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
7.0field-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

44 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Applications of Cannabinoids in Neuropathic Pain: An Updated Review.Critical reviews in therapeutic drug carrier systems · 2024
    Review
  5. Role of Cannabinoid Signaling in Cardiovascular Function and Ischemic Injury.The Journal of pharmacology and experimental therapeutics · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Targeting of G-protein coupled receptors in sepsis.Pharmacology & therapeutics · 2020
    Review
  12. Article
  13. Article
  14. Endocannabinoid System in the Airways.Molecules (Basel, Switzerland) · 2019
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  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

12 authors at 5 institutions in 2 countries.

Partha MukhopadhyayLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Bėla Horváth
Mohanraj Rajesh
Shingo Matsumoto
Keita Saito
Sándor Bátkai
Vivek Patel
Galin Tanchian
Rachel Y Gao
Benjamin F Cravatt
György Haskó
Pál Pacher
National Cancer Institute · USNational Institute on Alcohol Abuse and Alcoholism · USNational Institutes of Health · USRutgers New Jersey Medical SchoolScripps Research Institute · US

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZ01AA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2006 to 2008
$1.3M
Intramural NIH HHS Z01 AA000375Intramural NIH HHS Z99 AA999999Intramural NIH HHS ZIA AA000375
6 · The paper itself

Abstract

Previous studies have suggested that increased levels of endocannabinoids in various cardiovascular disorders (e.g., various forms of shock, cardiomyopathies, atherosclerosis) through the activation of CB(1) cannabinoid receptors may promote cardiovascular dysfunction and tissue injury. We have investigated the role of the main endocannabinoid anandamide-metabolizing enzyme (fatty acid amide hydrolase; FAAH) in myocardial injury induced by an important chemotherapeutic drug, doxorubicin (DOX; known for its cardiotoxicity mediated by increased reactive oxygen and nitrogen species generation), using well-established acute and chronic cardiomyopathy models in mice. The DOX-induced myocardial oxidative/nitrative stress (increased 4-hydroxynonenal, protein carbonyl, and nitrotyrosine levels and decreased glutathione content) correlated with multiple cell death markers, which were enhanced in FAAH knockout mice exhibiting significantly increased DOX-induced mortality and cardiac dysfunction compared to their wild type. The effects of DOX in FAAH knockouts were attenuated by CB(1) receptor antagonists. Furthermore, anandamide induced enhanced cell death in human cardiomyocytes pretreated with FAAH inhibitor and enhanced sensitivity to ROS generation in inflammatory cells of FAAH knockouts. These results suggest that in pathological conditions associated with acute oxidative/nitrative stress FAAH plays a key role in controlling the tissue injury that is, at least in part, mediated by the activation of CB(1) receptors by endocannabinoids.

Indexed as

EndocannabinoidsAmidohydrolasesAnimalsAntineoplastic AgentsCannabinoid Receptor ModulatorsCardiomyopathiesCells, CulturedDoxorubicinFatty Acid Amide HydrolasesHeartHumansMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumAmidohydrolasesAntineoplastic AgentsCannabinoid Receptor ModulatorsDoxorubicinEndocannabinoidsFatty Acid Amide HydrolasesReactive Oxygen SpeciesReceptor, Cannabinoid, CB1

Identifiers

PMID21070851
PMCPMC3022384
OpenAlexW2016318917

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.