Evidence map›Paper›PMID 32129826›Full record

ReviewBiochemical Society transactions2020

Exaggerated mitophagy: a weapon of striatal destruction in the brain?

Srinivasa Subramaniam

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The role of autophagy in death of cardiomyocytes.Journal of molecular and cellular cardiology · 2022
    Review
  6. Review
  7. Review
  8. Neuronal Mitophagy: Friend or Foe?Frontiers in cell and developmental biology · 2020
    Review
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

1 author at 1 institution in 1 country.

Srinivasa SubramaniamDepartment of Neuroscience, The Scripps Research Institute, Jupiter, FL 33458, U.S.A.
Scripps Research Institute · US

Funding

mTOR Signaling in Striatum: Regulation and FunctionR01NS087019 · NINDS · SCRIPPS FLORIDA · PI SUBRAMANIAM, SRINI · 2015 to 2019
$2.3M
Rhes-SUMO circuitry in Huntington's Disease PathogenesisR01NS094577 · NINDS · SCRIPPS FLORIDA · PI SUBRAMANIAM, SRINI · 2016 to 2019
$1.7M
NINDS NIH HHS R01 NS087019NINDS NIH HHS R01 NS094577
6 · The paper itself

Abstract

Mechanisms responsible for neuronal vulnerability in the brain remain unclear. Striatal neurons are preferentially damaged by 3-nitropropionic acid (3-NP), a mitochondrial complex-II inhibitor, causing striatal damage reminiscent of Huntington's disease (HD), but the mechanisms of the selectivity are not as well understood. We have discovered that Rhes, a protein enriched in the striatum, removes mitochondria via the mitophagy process. The process becomes intensified in the presence of 3-NP, thereby eliminating most of the mitochondria from the striatum. We put forward the hypothesis that Rhes acts as a 'mitophagy ligand' in the brain and promotes mitophagy via NIX, a mitophagy receptor. Since Rhes interacts and promotes toxicity in association with mutant huntingtin (mHTT), the genetic cause of HD, it is tempting to speculate on whether the exaggerated mitophagy may be a contributing factor to the striatal lesion found in HD. Thus, Rhes-mediated exaggerated mitophagy may act as a weapon of striatal destruction in the brain.

Indexed as

MitophagyAnimalsBrainCorpus StriatumDrug DevelopmentHippocampusHumansHuntingtin ProteinHuntington DiseaseLysosomesMembrane ProteinsMitochondriaNeuronsNitro CompoundsPropionatesProtein Domains3-nitropropionic acidBNIP3 protein, humanHTT protein, humanHuntingtin ProteinMembrane ProteinsNitro CompoundsPropionatesProto-Oncogene Proteinslesionlysosomesmitochondrial damageselectivitystriatumtoxin

Identifiers

PMID32129826
PMCPMC7200642
OpenAlexW3009422216

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.