Evidence map›Paper›PMID 36671032›Full record

ReviewAntioxidants (Basel, Switzerland)2023

The Dual Role of Oxidative-Stress-Induced Autophagy in Cellular Senescence: Comprehension and Therapeutic Approaches.

Pavlos Pantelis, George Theocharous, Nefeli Lagopati, Dimitris Veroutis, Dimitris-Foivos Thanos, Giasemi-Panagiota Lampoglou, Natassa Pippa, Maria-Anna Gatou, Ioanna Tremi, Angelos Papaspyropoulos and 5 more

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.5field-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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  8. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
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  11. Article
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  16. The Critical Role of Autophagy and Phagocytosis in the Aging Brain.International journal of molecular sciences · 2024
    Review
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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

15 authors at 3 institutions in 2 countries.

Pavlos PantelisMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
George TheocharousMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Nefeli LagopatiMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Dimitris VeroutisMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Dimitris-Foivos ThanosMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Giasemi-Panagiota LampoglouMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Natassa PippaSection of Pharmaceutical Technology, Department of Pharmacy, School of Health Sciences, National and Kapodistrian University of Athens, 15771 Athens, Greece.
Maria-Anna GatouLaboratory of General Chemistry, School of Chemical Engineering, National Technical University of Athens, 6 Zografou Campus, 15789 Zografou, Greece.
Ioanna TremiMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Angelos PapaspyropoulosMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Efthymios KyrodimosFirst ENT Department, Hippocration Hospital, University of Athens, 11527 Athens, Greece.
Evangelia A PavlatouLaboratory of General Chemistry, School of Chemical Engineering, National Technical University of Athens, 6 Zografou Campus, 15789 Zografou, Greece.
Maria GazouliLaboratory of Biology, Department of Basic Medical Sciences, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-3295-6811
Konstantinos EvangelouMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.
Vassilis G GorgoulisMolecular Carcinogenesis Group, Department of Histology and Embryology, Medical School, National Kapodistrian University of Athens (NKUA), 11527 Athens, Greece.ORCID 0000-0001-9001-4112
National and Kapodistrian University of Athens · GRNational Technical University of Athens · GRUniversity of Dundee · GB

Funding

European Regional Development Fund of the European Union and Greek national funds through the Operational Program Competitiveness, Entrepreneurship and Innovation, under the call RESEARCH - CREATE - INNOVATE Τ2EDK-02939
6 · The paper itself

Abstract

The contemporary lifestyle of the last decade has undeniably caused a tremendous increase in oxidative-stress-inducing environmental sources. This phenomenon is not only connected with the rise of ROS levels in multiple tissues but is also associated with the induction of senescence in different cell types. Several signaling pathways that are associated with the reduction in ROS levels and the regulation of the cell cycle are being activated, so that the organism can battle deleterious effects. Within this context, autophagy plays a significant role. Through autophagy, cells can maintain their homeostasis, as if it were a self-degradation process, which removes the "wounded" molecules from the cells and uses their materials as a substrate for the creation of new useful cell particles. However, the role of autophagy in senescence has both a "dark" and a "bright" side. This review is an attempt to reveal the mechanistic aspects of this dual role. Nanomedicine can play a significant role, providing materials that are able to act by either preventing ROS generation or controllably inducing it, thus functioning as potential therapeutic agents regulating the activation or inhibition of autophagy.

Indexed as

autophagycellular senescencelipofuscinmacroautophagymacromolecular damageoxidative stressROS pathwaysSASP

Identifiers

PMID36671032
PMCPMC9854717
OpenAlexW4315567599

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.