Evidence map›Paper›PMID 28695466›Full record

ArticleJournal of physiology and biochemistry2017

Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.

Anja Petrović, Desanka Bogojević, Aleksandra Korać, Igor Golić, Sofija Jovanović-Stojanov, Vesna Martinović, Svetlana Ivanović-Matić, Jelena Stevanović, Goran Poznanović, Ilijana Grigorov

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Article in Journal of physiology and biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Involvement of Ferroptosis in Diabetes-Induced Liver Pathology.International journal of molecular sciences · 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

10 authors at 1 institution in 1 country.

Anja PetrovićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Desanka BogojevićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Aleksandra KoraćFaculty of Biology, Center for Electron Microscopy, University of Belgrade, Belgrade, Serbia.
Igor GolićFaculty of Biology, Center for Electron Microscopy, University of Belgrade, Belgrade, Serbia.
Sofija Jovanović-StojanovDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Vesna MartinovićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Svetlana Ivanović-MatićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Jelena StevanovićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Goran PoznanovićDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia.
Ilijana GrigorovDepartment of Molecular Biology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Bulevar despota Stefana 142, Republic of Belgrade, 11060, Serbia. iligri@ibiss.bg.ac.rs.
University of Belgrade · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The progression of oxidative stress, resulting cell damage, and cell death underlies the etiology of liver damage/dysfunction as a complication of diabetes. High-mobility group box 1 (HMGB1) protein, a chromatin-binding nuclear protein and damage-associated molecular pattern molecule, is integral to oxidative stress and signaling pathways regulating cell death and cell survival. We previously found that in streptozotocin (STZ)-induced diabetic rats, reduction of oxidative stress after melatonin administration lowered necrotic cell death and increased expression of HMGB1 and hepatocellular damage. In the present study, we examined whether alleviation of diabetes-attendant oxidative stress and ensuing change in HMGB1 expression influence the dynamic equilibrium between apoptosis/autophagy and liver damage. We observed that elevated HMGB1 protein levels in diabetic rat liver accompanied increased interactions of HMGB1 with TLR4 and RAGE, and activation of the intrinsic apoptotic pathway and Beclin 1-dependent autophagy. The absence of p62 degradation in diabetic rat liver pointed to defective autophagy which was responsible for lower autophagosome/autophagolysosome formation and an increased apoptosis/autophagy ratio. Compared to diabetic rats, in melatonin-treated diabetic rats, the structure of liver cells was preserved, HMGB1/TLR4 interaction and downstream apoptotic signaling were significantly reduced, HMGB1/Beclin 1 colocalization and interactions were augmented and Beclin 1-mediated autophagy, mithophagy in particular, were increased. We concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage. Since reduced HMGB1 binds to RAGE but not to TLR4, redox modification of HMGB1 as a mechanism regulating the cross-talk between apoptosis and autophagy in diabetes is discussed.

Indexed as

Oxidative StressAnimalsApoptosisAutophagyDiabetes Mellitus, ExperimentalHMGB1 ProteinLiverRatsHbp1 protein, ratHMGB1 ProteinApoptosis/autophagy interplayDiabetesHMGB1Liver damageMelatoninOxidative stress

Identifiers

PMID28695466
OpenAlexW2735592915

What OpenQuestion holds

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Registered trials

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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.