Evidence map›Paper›PMID 37576343›Full record

ReviewFrontiers in physiology2023

Exploring the therapeutic potential of the mitochondrial transfer-associated enzymatic machinery in brain degeneration.

Noymar Luque-Campos, Ricardo Riquelme, Luis Molina, Gisela Canedo-Marroquín, Ana María Vega-Letter, Patricia Luz-Crawford, Felipe A Bustamante-Barrientos

Erratum issuedAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Noymar Luque-CamposLaboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile.
Ricardo RiquelmeEscuela de Nutrición y Dietética, Facultad de Medicina, Universidad de los Andes, Santiago, Chile.
Luis MolinaFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Gisela Canedo-MarroquínCentro de Investigación e Innovación Biomédica, Universidad de los Andes, Santiago, Chile.
Ana María Vega-LetterEscuela de Ingeniería Bioquímica, Pontificia Universidad Católica de Valparaiso, Valparaiso, Chile.
Patricia Luz-CrawfordLaboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile.
Felipe A Bustamante-BarrientosLaboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is a central event in the pathogenesis of several degenerative brain disorders. It entails fission and fusion dynamics disruption, progressive decline in mitochondrial clearance, and uncontrolled oxidative stress. Many therapeutic strategies have been formulated to reverse these alterations, including replacing damaged mitochondria with healthy ones. Spontaneous mitochondrial transfer is a naturally occurring process with different biological functions. It comprises mitochondrial donation from one cell to another, carried out through different pathways, such as the formation and stabilization of tunneling nanotubules and Gap junctions and the release of extracellular vesicles with mitochondrial cargoes. Even though many aspects of regulating these mechanisms still need to be discovered, some key enzymatic regulators have been identified. This review summarizes the current knowledge on mitochondrial dysfunction in different neurodegenerative disorders. Besides, we analyzed the usage of mitochondrial transfer as an endogenous revitalization tool, emphasizing the enzyme regulators that govern this mechanism. Going deeper into this matter would be helpful to take advantage of the therapeutic potential of mitochondrial transfer.

Indexed as

cellular therapydegenerative brain disordersenzymesfission and fusionmitochondrial dysfunctionmitochondrial transfermitophagyoxidative damage

Identifiers

PMID37576343
PMCPMC10416799

What OpenQuestion holds

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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.