Evidence map›Paper›PMID 34829705›Full record

ReviewAntioxidants (Basel, Switzerland)2021

TRAP1 in Oxidative Stress and Neurodegeneration.

Inês Ramos Rego, Beatriz Santos Cruz, António Francisco Ambrósio, Celso Henrique Alves

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  8. Article
  9. TRAP1 and its therapeutic potential.Bioorganic & medicinal chemistry letters · 2025
    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

4 authors at 2 institutions in 1 country.

Inês Ramos RegoRetinal Dysfunction and Neuroinflammation Lab, Faculty of Medicine, Coimbra Institute for Clinical and Biomedical Research (iCBR), University Coimbra, 3000-548 Coimbra, Portugal.ORCID 0000-0002-6152-3468
Beatriz Santos CruzRetinal Dysfunction and Neuroinflammation Lab, Faculty of Medicine, Coimbra Institute for Clinical and Biomedical Research (iCBR), University Coimbra, 3000-548 Coimbra, Portugal.
António Francisco AmbrósioRetinal Dysfunction and Neuroinflammation Lab, Faculty of Medicine, Coimbra Institute for Clinical and Biomedical Research (iCBR), University Coimbra, 3000-548 Coimbra, Portugal.ORCID 0000-0002-0477-1641
Celso Henrique AlvesRetinal Dysfunction and Neuroinflammation Lab, Faculty of Medicine, Coimbra Institute for Clinical and Biomedical Research (iCBR), University Coimbra, 3000-548 Coimbra, Portugal.ORCID 0000-0001-9776-5701
Association for Innovation and Biomedical Research on Light and Image · PTUniversity of Coimbra · PT

Funding

Fundação para a Ciência e Tecnologia CEECIND/00886/2017Fundação para a Ciência e Tecnologia Centro 2020 Regional Operational Programme (CENTRO-01-0145-FEDER-000008: BrainHealth 2020)Fundação para a Ciência e Tecnologia Strategic Project UIDB/04539/2020 and UIDP/04539/2020 (CIBB),
6 · The paper itself

Abstract

Tumor necrosis factor receptor-associated protein 1 (TRAP1), also known as heat shock protein 75 (HSP75), is a member of the heat shock protein 90 (HSP90) chaperone family that resides mainly in the mitochondria. As a mitochondrial molecular chaperone, TRAP1 supports protein folding and contributes to the maintenance of mitochondrial integrity even under cellular stress. TRAP1 is a cellular regulator of mitochondrial bioenergetics, redox homeostasis, oxidative stress-induced cell death, apoptosis, and unfolded protein response (UPR) in the endoplasmic reticulum (ER). TRAP1 has attracted increasing interest as a therapeutical target, with a special focus on the design of TRAP1 specific inhibitors. Although TRAP1 was extensively studied in the oncology field, its role in central nervous system cells, under physiological and pathological conditions, remains largely unknown. In this review, we will start by summarizing the biology of TRAP1, including its structure and related pathways. Thereafter, we will continue by debating the role of TRAP1 in the maintenance of redox homeostasis and protection against oxidative stress and apoptosis. The role of TRAP1 in neurodegenerative disorders will also be discussed. Finally, we will review the potential of TRAP1 inhibitors as neuroprotective drugs.

Indexed as

HSP75HSP90mitochondrianeurodegenerationoxidative stressTRAP1

Identifiers

PMID34829705
PMCPMC8614808
OpenAlexW3214004285

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.