Evidence map›Paper›PMID 27330055›Full record

ReviewJournal of lipid research2016

Lipid signaling and lipotoxicity in metaflammation: indications for metabolic disease pathogenesis and treatment.

Meric Erikci Ertunc, Gökhan S Hotamisligil

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 1 pooled it
29.6field-weighted citation impact, top 1% 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

224 citing papers in PubMed, 1 synthesis or guideline pooled it, 466 citations in OpenAlex.

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  14. An Aqueous Extract ofInternational journal of molecular sciences · 2026
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164 more citing papers are in PubMed but not listed here.

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.

Meric Erikci ErtuncDepartment of Genetics and Complex Diseases and Sabri Ülker Center, Harvard T. H. Chan School of Public Health, Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, MA 02115.
Gökhan S HotamisligilDepartment of Genetics and Complex Diseases and Sabri Ülker Center, Harvard T. H. Chan School of Public Health, Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, MA 02115. Electronic address: ghotamis@hsph.harvard.edu.
Massachusetts Institute of Technology · US

Funding

TNF RECEPTOR FUNCTION IN INSULIN RESISTANCE AND OBESITYR01DK052539 · NIDDK · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI HOTAMISLIGIL, GOKHAN S · 1998 to 2017
$6.8M
The role of fatty acid binding protein aP2 in the pathogenesis and treatment of asthmaR01AI116901 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI HOTAMISLIGIL, GOKHAN S · 2015 to 2018
$1.6M
The role of immunometabolic pathways in atherosclerosisR01HL125753 · NHLBI · HARVARD SCHOOL OF PUBLIC HEALTH · PI HOTAMISLIGIL, GOKHAN S · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL125753NIAID NIH HHS R01 AI116901NIDDK NIH HHS R01 DK052539
6 · The paper itself

Abstract

Lipids encompass a wide variety of molecules such as fatty acids, sterols, phospholipids, and triglycerides. These molecules represent a highly efficient energy resource and can act as structural elements of membranes or as signaling molecules that regulate metabolic homeostasis through many mechanisms. Cells possess an integrated set of response systems to adapt to stresses such as those imposed by nutrient fluctuations during feeding-fasting cycles. While lipids are pivotal for these homeostatic processes, they can also contribute to detrimental metabolic outcomes. When metabolic stress becomes chronic and adaptive mechanisms are overwhelmed, as occurs during prolonged nutrient excess or obesity, lipid influx can exceed the adipose tissue storage capacity and result in accumulation of harmful lipid species at ectopic sites such as liver and muscle. As lipid metabolism and immune responses are highly integrated, accumulation of harmful lipids or generation of signaling intermediates can interfere with immune regulation in multiple tissues, causing a vicious cycle of immune-metabolic dysregulation. In this review, we summarize the role of lipotoxicity in metaflammation at the molecular and tissue level, describe the significance of anti-inflammatory lipids in metabolic homeostasis, and discuss the potential of therapeutic approaches targeting pathways at the intersection of lipid metabolism and immune function.

Indexed as

Lipid MetabolismAdipose TissueAnimalsEnergy MetabolismHumansInflammation MediatorsInsulin ResistanceLiverMetabolic DiseasesMuscle, SkeletalStress, PhysiologicalInflammation Mediatorsdiabetesinflammationinsulin resistancelipidsobesitysignaling lipids

Identifiers

PMID27330055
PMCPMC5321214
OpenAlexW2461706302

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.