Evidence map›Paper›PMID 29725497›Full record

ReviewOxidative medicine and cellular longevity2018

Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction.

Giuseppina Amodio, Ornella Moltedo, Raffaella Faraonio, Paolo Remondelli

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

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  9. New Frontiers on ER Stress Modulation: Are TRP Channels the Leading Actors?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

4 authors at 2 institutions in 1 country.

Giuseppina AmodioDipartimento di Medicina, Chirurgia e Odontoiatria "Scuola Medica Salernitana", Università degli Studi di Salerno, 84081 Baronissi, Italy.ORCID 0000-0001-8971-8964
Ornella MoltedoDipartimento di Farmacia, Università degli Studi di Salerno, 84084 Fisciano, Italy.
Raffaella FaraonioDipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli studi di Napoli "Federico II", 80131 Naples, Italy.
Paolo RemondelliDipartimento di Medicina, Chirurgia e Odontoiatria "Scuola Medica Salernitana", Università degli Studi di Salerno, 84081 Baronissi, Italy.ORCID 0000-0002-3698-3497
University of Salerno · ITCeinge Biotecnologie Avanzate (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the UPR pathways is the promotion of an adaptive response, the persistent activation of UPR leads to increased oxidative stress and cell death. This molecular switch has been correlated to the onset or to the exacerbation of the endothelial dysfunction in cardiovascular diseases. In this review, we highlight the multiple chances of the UPR to induce or ameliorate oxidative disturbances and propose the UPR pathways as a new therapeutic target for the clinical management of endothelial dysfunction.

Indexed as

Endoplasmic ReticulumEndothelial CellsHumansOxidative StressUnfolded Protein Response

Identifiers

PMID29725497
PMCPMC5872601
OpenAlexW2790643739

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.