Evidence map›Paper›PMID 24807843›Full record

ReviewCell biochemistry and biophysics2014

Autophagy of mitochondria: a promising therapeutic target for neurodegenerative disease.

Pradip K Kamat, Anuradha Kalani, Philip Kyles, Suresh C Tyagi, Neetu Tyagi

Abstract readReview
In one paragraph

Review in Cell biochemistry and biophysics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  8. Ablation ofbioRxiv : the preprint server for biology · 2023
    Article
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  18. New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021
    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

5 authors at 2 institutions in 1 country.

Pradip K KamatDepartment of Physiology and Biophysics, School of Medicine, Health Sciences Center, University of Louisville, A-1201, Louisville, KY, 40202, USA.
Anuradha Kalani
Philip Kyles
Suresh C Tyagi
Neetu Tyagi
University of Louisville · USUniversity of Louisville Hospital · US

Funding

Mechanisms of Mitochondrial Dysfunction in Brain VasculatureR01HL107640 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, NEETU · 2012 to 2016
$1.8M
Mechanisms of Cerebral Vascular RemodelingR01NS051568 · NINDS · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2007 to 2011
$1.6M
NHLBI NIH HHS HL107640NHLBI NIH HHS R01 HL107640NINDS NIH HHS R01 NS051568
6 · The paper itself

Abstract

The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is associated with cellular oxidative stress and its impact on neurodegeneration. This impaired autophagic function may be considered as a possible mechanism in the pathogenesis of several neurodegenerative disorders including Parkinson's disease, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington disease. It can be suggested that autophagy dysfunction along with oxidative stress is considered main events in neurodegenerative disorders. New therapeutic approaches have now begun to target mitochondria as a potential drug target. This review discusses evidence supporting the notion that oxidative stress and autophagy are intimately associated with neurodegenerative disease pathogenesis. This review also explores new approaches that can prevent mitochondrial dysfunction, improve neurodegenerative etiology, and also offer possible cures to the aforementioned neurodegenerative diseases.

Indexed as

AnimalsAutophagyHumansMitochondriaMolecular Targeted TherapyNeurodegenerative Diseases

Identifiers

PMID24807843
PMCPMC4184921
OpenAlexW2078643780

What OpenQuestion holds

Textmetadata
LicenceTDM
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.