Evidence map›Paper›PMID 29316632›Full record

ArticleInternational journal of molecular sciences2018

Excessive Endoplasmic Reticulum Stress Correlates with Impaired Mitochondrial Dynamics, Mitophagy and Apoptosis, in Liver and Adipose Tissue, but Not in Muscles in EMS Horses.

Krzysztof Marycz, Katarzyna Kornicka, Jolanta Szlapka-Kosarzewska, Christine Weiss

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 68 citations in OpenAlex.

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  13. GRP78 Activity Moderation as a Therapeutic Treatment against Obesity.International journal of environmental research and public health · 2022
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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

4 authors at 1 institution in 1 country.

Krzysztof MaryczDepartment of Experimental Biology, Wroclaw University of Environmental and Life Sciences, 50-375 Wroclaw, Poland. krzysztof.marycz@upwr.edu.pl.ORCID 0000-0003-3676-796X
Katarzyna KornickaDepartment of Experimental Biology, Wroclaw University of Environmental and Life Sciences, 50-375 Wroclaw, Poland. kornicka.katarzyna@gmail.com.
Jolanta Szlapka-KosarzewskaDepartment of Experimental Biology, Wroclaw University of Environmental and Life Sciences, 50-375 Wroclaw, Poland. jolanta.szlapka@gmail.com.
Christine WeissPferdePraxis Dr. Med. Vet. Daniel Weiss, Postmatte 14, CH-8807 Freienbach, Switzerland. d.weiss@horsedoc.ch.
Wrocław University of Environmental and Life Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nowadays, endocrine disorders have become more frequent in both human and veterinary medicine. In horses, reduced physical activity combined with carbohydrate and sugar overload may result in the development of the so-called equine metabolic syndrome (EMS). EMS is characterized by insulin resistance, hyperinsulinemia, elevated blood triglyceride concentrations and usually obesity. Although the phenotypic features of EMS individuals are well known, the molecular mechanism underlying disease development remains elusive. Therefore, in the present study, we analyzed insulin-sensitive tissues, i.e., muscles, liver and adipose tissue in order to evaluate insulin resistance and apoptosis. Furthermore, we assessed mitochondrial dynamics and mitophagy in those tissues, because mitochondrial dysfunction is linked to the development of metabolic syndrome. We established the expression of genes related to insulin resistance, endoplasmic reticulum (ER) stress and mitochondria clearance by mitophagy using RT-PCR and Western blot. Cell ultrastructure was visualized using electron transmission microscopy. The results indicated that adipose tissue and liver of EMS horses were characterized by increased mitochondrial damage and mitophagy followed by triggering of apoptosis as mitophagy fails to restore cellular homeostasis. However, in muscles, apoptosis was reduced, suggesting the existence of a protective mechanism allowing that tissue to maintain homeostasis.

Indexed as

ApoptosisEndoplasmic Reticulum StressMitophagyAdipose TissueAnimalsCytokineseIF-2 KinaseHorsesInsulin ResistanceLiverMetabolic SyndromeMicroscopy, Electron, TransmissionMitochondriaMitochondrial DynamicsMuscle, SkeletalOxidative StressCytokineseIF-2 Kinaseparkin proteinReactive Oxygen SpeciesSuperoxide DismutaseTranscription Factor CHOPUbiquitin-Protein Ligasesapoptosisautophagyinsulin resistancemetabolic syndromemitochondria

Identifiers

PMID29316632
PMCPMC5796114
OpenAlexW2783418499

What OpenQuestion holds

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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.