Evidence map›Paper›PMID 35163080›Full record

ArticleInternational journal of molecular sciences2022

PEG35 as a Preconditioning Agent against Hypoxia/Reoxygenation Injury.

Rui Teixeira da Silva, Ivo F Machado, João S Teodoro, Arnau Panisello-Roselló, Joan Roselló-Catafau, Anabela P Rolo, Carlos M Palmeira

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-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

8 citing papers in PubMed, 18 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

7 authors at 2 institutions in 2 countries.

Rui Teixeira da SilvaDepartment of Life Sciences, University of Coimbra, 3000-456 Coimbra, Portugal.ORCID 0000-0001-7274-4007
Ivo F MachadoCenter for Neurosciences and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal.ORCID 0000-0002-9666-4594
João S TeodoroDepartment of Life Sciences, University of Coimbra, 3000-456 Coimbra, Portugal.ORCID 0000-0002-1244-275X
Arnau Panisello-RosellóExperimental Pathology Department, Institute of Biomedical Research of Barcelona (IIBB), CSIC-IDIBAPS, 08036 Barcelona, Spain.
Joan Roselló-CatafauExperimental Pathology Department, Institute of Biomedical Research of Barcelona (IIBB), CSIC-IDIBAPS, 08036 Barcelona, Spain.
Anabela P RoloDepartment of Life Sciences, University of Coimbra, 3000-456 Coimbra, Portugal.
Carlos M PalmeiraDepartment of Life Sciences, University of Coimbra, 3000-456 Coimbra, Portugal.ORCID 0000-0002-2639-7697
University of Coimbra · PTInstitut d'Investigacions Biomèdiques de Barcelona · ES

Funding

European Regional Development Fund CENTRO-01-0145-FEDER-000012European Union 722619Fundação para a Ciência e a Tecnologia POCI-01-0145-FEDER-016770
6 · The paper itself

Abstract

Pharmacological conditioning is a protective strategy against ischemia/reperfusion injury, which occurs during liver resection and transplantation. Polyethylene glycols have shown multiple benefits in cell and organ preservation, including antioxidant capacity, edema prevention and membrane stabilization. Recently, polyethylene glycol 35 kDa (PEG35) preconditioning resulted in decreased hepatic injury and protected the mitochondria in a rat model of cold ischemia. Thus, the study aimed to decipher the mechanisms underlying PEG35 preconditioning-induced protection against ischemia/reperfusion injury. A hypoxia/reoxygenation model using HepG2 cells was established to evaluate the effects of PEG35 preconditioning. Several parameters were assessed, including cell viability, mitochondrial membrane potential, ROS production, ATP levels, protein content and gene expression to investigate autophagy, mitochondrial biogenesis and dynamics. PEG35 preconditioning preserved the mitochondrial function by decreasing the excessive production of ROS and subsequent ATP depletion, as well as by recovering the membrane potential. Furthermore, PEG35 increased levels of autophagy-related proteins and the expression of genes involved in mitochondrial biogenesis and fusion. In conclusion, PEG35 preconditioning effectively ameliorates hepatic hypoxia/reoxygenation injury through the enhancement of autophagy and mitochondrial quality control. Therefore, PEG35 could be useful as a potential pharmacological tool for attenuating hepatic ischemia/reperfusion injury in clinical practice.

Indexed as

AutophagyHumansHypoxiaIschemic PreconditioningLiverMembrane Potential, MitochondrialMitochondriaPolyethylene GlycolsProtective AgentsReperfusion InjuryPolyethylene GlycolsProtective Agentsautophagyhypoxia/reoxygenation injurymitochondriapolyethylene glycol 35

Identifiers

PMID35163080
PMCPMC8834864
OpenAlexW4206615529

What Socratic 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 Socratic graph.