Evidence map›Paper›PMID 35008640›Full record

ArticleInternational journal of molecular sciences2021

AICAR Protects Vascular Endothelial Cells from Oxidative Injury Induced by the Long-Term Palmitate Excess.

Mikhail V Samsonov, Nikita V Podkuychenko, Asker Y Khapchaev, Eugene E Efremov, Elena V Yanushevskaya, Tatiana N Vlasik, Vadim Z Lankin, Iurii S Stafeev, Maxim V Skulachev, Marina V Shestakova and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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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 3 institutions in 1 country.

Mikhail V SamsonovNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Nikita V PodkuychenkoNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Asker Y KhapchaevNational Medical Research Center for Cardiology, 121552 Moscow, Russia.ORCID 0000-0001-7889-3337
Eugene E EfremovNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Elena V YanushevskayaNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Tatiana N VlasikNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Vadim Z LankinNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Iurii S StafeevNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
Maxim V SkulachevBelozersky Institute of Physico-Chemical Biology, M. V. Lomonosov Moscow State University, 119234 Moscow, Russia.
Marina V ShestakovaDiabetes Institute, Endocrinology Research Center, 117036 Moscow, Russia.
Alexander V VorotnikovNational Medical Research Center for Cardiology, 121552 Moscow, Russia.ORCID 0000-0002-1460-971X
Vladimir P ShirinskyNational Medical Research Center for Cardiology, 121552 Moscow, Russia.
National Medical Research Center of Cardiology · RUEndocrinology Research Center · RULomonosov Moscow State University · RU

Funding

Russian Science Foundation 19-15-00361
6 · The paper itself

Abstract

Hyperlipidemia manifested by high blood levels of free fatty acids (FFA) and lipoprotein triglycerides is critical for the progression of type 2 diabetes (T2D) and its cardiovascular complications via vascular endothelial dysfunction. However, attempts to assess high FFA effects in endothelial culture often result in early cell apoptosis that poorly recapitulates a much slower pace of vascular deterioration in vivo and does not provide for the longer-term studies of endothelial lipotoxicity in vitro. Here, we report that palmitate (PA), a typical FFA, does not impair, by itself, endothelial barrier and insulin signaling in human umbilical vein endothelial cells (HUVEC), but increases NO release, reactive oxygen species (ROS) generation, and protein labeling by malondialdehyde (MDA) hallmarking oxidative stress and increased lipid peroxidation. This PA-induced stress eventually resulted in the loss of cell viability coincident with loss of insulin signaling. Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA, thus allowing to maintain HUVEC viability and barrier, and providing the means to study the long-term effects of high FFA levels in endothelial cultures. An upgraded cell-based model reproduces FFA-induced insulin resistance by demonstrating decreased NO production by vascular endothelium.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesApoptosisCells, CulturedCell SurvivalEndothelium, VascularFatty Acids, NonesterifiedHumansHuman Umbilical Vein Endothelial CellsInsulinInsulin ResistanceLipid PeroxidationMalondialdehydeOxidative StressPalmitatesReactive Oxygen SpeciesAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesFatty Acids, NonesterifiedInsulinMalondialdehydePalmitatesReactive Oxygen SpeciesRibonucleotidesendothelial barrierHUVEChyperlipidemiainsulin signalingmalondialdehydeNOpalmitateROS

Identifiers

PMID35008640
PMCPMC8745318
OpenAlexW4200069336

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.