Evidence map›Paper›PMID 19622391›Full record

ReviewExperimental gerontology2009

Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders.

Mark P Mattson

Open access · greenAbstract readReview
In one paragraph

Review in Experimental gerontology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 2 pooled it
7.9field-weighted citation impact, top 2% 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

138 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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78 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

1 author at 1 institution in 1 country.

Mark P MattsonLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov
National Institute on Aging · US

Funding

Synaptic Plasticity In Aging And Neurodegenerative DisordersZIAAG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$8.5M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Apoptosis In Neurodegenerative DisordersZIAAG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Dietary Modification Of Brain Aging And Neurodegenerative DisordersZIAAG000315 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$5.0M
Dietary Modification Of Brain Aging /NeurodegenerativeZ01AG000315 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$2.0M
Cellular And Molecular Pathogenesis Of Alzheimer'sZ01AG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.9M
Synaptic Plasticity In Aging And Neurodegenerative DisordersZ01AG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.7M
Intramural NIH HHS Z01 AG000312Intramural NIH HHS Z01 AG000315Intramural NIH HHS Z01 AG000317
6 · The paper itself

Abstract

A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic beta cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.

Indexed as

AldehydesCross-Linking ReagentsDietHumansLipid PeroxidationMetabolic SyndromeNeurodegenerative DiseasesObesityOxidative StressVascular Diseases4-hydroxy-2-nonenalAldehydesCross-Linking Reagents

Identifiers

PMID19622391
PMCPMC2753676
OpenAlexW2090089932

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.