Evidence map›Paper›PMID 34356897›Full record

ReviewBiomedicines2021

Role of PITRM1 in Mitochondrial Dysfunction and Neurodegeneration.

Dario Brunetti, Alessia Catania, Carlo Viscomi, Michela Deleidi, Laurence A Bindoff, Daniele Ghezzi, Massimo Zeviani

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  5. The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
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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 5 institutions in 3 countries.

Dario BrunettiDepartment of Medical Biotechnology and Translational Medicine, University of Milan, 20129 Milan, Italy.ORCID 0000-0002-2740-9370
Alessia CataniaUnit of Medical Genetics and Neurogenetics, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20126 Milan, Italy.
Carlo ViscomiDepartment of Biomedical Sciences, University of Padova, 35131 Padova, Italy.
Michela DeleidiGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Laurence A BindoffNeuro-SysMed, Center of Excellence for Clinical Research in Neurological Diseases, Haukeland University Hospital, N-5021 Bergen, Norway.
Daniele GhezziUnit of Medical Genetics and Neurogenetics, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20126 Milan, Italy.ORCID 0000-0002-6564-3766
Massimo ZevianiDepartment of Neurosciences, University of Padova, 35128 Padova, Italy.ORCID 0000-0002-9067-5508
University of Milan · ITUniversity of Padua · ITFondazione IRCCS Istituto Neurologico Carlo Besta · ITGerman Center for Neurodegenerative Diseases · DEHaukeland University Hospital · NO

Funding

Fondazione Telethon GGP19007Fondazione Telethon GGP20013Fondazione Telethon GSP20003_PAsAtaxia002Helmholtz Association Young Investigator Award VH-NG-1123Università degli Studi di Milano SoE-SEED2020_MI.to.AD
6 · The paper itself

Abstract

Mounting evidence shows a link between mitochondrial dysfunction and neurodegenerative disorders, including Alzheimer Disease. Increased oxidative stress, defective mitodynamics, and impaired oxidative phosphorylation leading to decreased ATP production, can determine synaptic dysfunction, apoptosis, and neurodegeneration. Furthermore, mitochondrial proteostasis and the protease-mediated quality control system, carrying out degradation of potentially toxic peptides and misfolded or damaged proteins inside mitochondria, are emerging as potential pathogenetic mechanisms. The enzyme pitrilysin metallopeptidase 1 (PITRM1) is a key player in these processes; it is responsible for degrading mitochondrial targeting sequences that are cleaved off from the imported precursor proteins and for digesting a mitochondrial fraction of amyloid beta (Aβ). In this review, we present current evidence obtained from patients with

Indexed as

Alzheimer Diseasemitochondrial dysfunctionmitochondrial protein quality controlmitochondrial proteostasisneurodegenerationneurodegenerative dementianeurodegenerative diseasespitrilysin metallopeptidase 1PITRM1protein aggregationspinocerebellar ataxia

Identifiers

PMID34356897
PMCPMC8301332
OpenAlexW3183806972

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.