Evidence map›Paper›PMID 29237272›Full record

ArticleAntioxidants & redox signaling2018

Bioactive Lipids and Redox Signaling: Molecular Mechanism and Disease Pathogenesis.

Pin-Lan Li, Erich Gulbins

Abstract readEditorial
In one paragraph

Article in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium.International journal of molecular sciences · 2021
    Review
  10. Review
  11. A dual role of 12/15-lipoxygenase in LPS-induced acute renal inflammation and injury.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Article
  12. Article
  13. Article
  14. Ceramide and Regulation of Vascular Tone.International journal of molecular sciences · 2019
    Review
  15. Review
  16. 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 2 countries.

Pin-Lan LiDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, Virginia.
Erich GulbinsInstitute of Molecular Biology, University of Duisburg-Essen, Essen, Germany.
Institute of Molecular Biology · DEVirginia Commonwealth University · US

Funding

Regulation of Lysosomes in Autophagy in Coronary Arterial MyocytesR01HL057244 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2001 to 2021
$6.7M
Subendothelial Exosomes in Coronary Microvascular DysfunctionR01HL075316 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2004 to 2024
$6.7M
Hypertension and glomerular injury in hyperhomocysteinemia - role of inflammatory exosomesR01DK054927 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 1998 to 2023
$6.7M
Lysosome dysfunction in podocytopathy and associated hypertensionR01DK120491 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2018 to 2022
$2.4M
NAADP-Sensitive Lysosomal Ca2+ Release Channels-TRP-ML1 in Arterial MyocytesR01HL091464 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2009 to 2013
$2.2M
NHLBI NIH HHS R01 HL057244NHLBI NIH HHS R01 HL075316NHLBI NIH HHS R01 HL091464NIDDK NIH HHS R01 DK054927NIDDK NIH HHS R01 DK120491
6 · The paper itself

Abstract

The actions of bioactive lipids and reactive oxygen species (ROS) are usually coupled, and their interplay is a common and important mechanism mediating tissue injury, inflammation, and other pathologies. Understanding the interplay of ROS and lipid mediators will extend horizons for researchers to clarify the pathogenesis of different diseases and help identify therapeutic targets for treatment of these diseases. Some bioactive lipids are converted into oxidized lipids during cell or tissue oxidative stress such as isoprostanes and isoketals, which are even more bioactive than their precursors. Moreover, many enzymes that produce lipid mediators such as prostaglandin H synthases, lipoxygenases, and cytochrome P450 isoforms may catalyze the production of ROS. Bioactive lipids-lysophospholipids, sphingolipids, or deposited lipids in cells-are shown to stimulate redox enzymes to produce ROS. In addition, a lipid-channel-ROS axis in different organelles may be associated with the crosstalk of ROS and bioactive lipids. This Forum focuses on the crosstalk of ROS with sphingolipids, P450 eicosanoids, lysophospholipids, and deposited plasma lipids and related novel signaling pathway in their reciprocal actions, which is expected to provide novel insights into the pathogenesis of different diseases associated with the participation of these lipid mediators. It is imperative to further understand the molecular mechanism mediating the crosstalk of ROS with specific lipid mediators and to develop more effective therapeutic strategies to target the interplay of ROS and lipid mediators for treatment specific to different organ diseases.

Indexed as

ceramideeicosanoidslipid mediatorslysophospholipidsROSsphingolipids

Identifiers

PMID29237272
PMCPMC5849277
OpenAlexW2771652025

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.