Evidence map›Paper›PMID 29364506›Full record

ReviewFEBS letters2018

The mitochondrial transcription factor TFAM in neurodegeneration: emerging evidence and mechanisms.

Inhae Kang, Charleen T Chu, Brett A Kaufman

Open access · greenAbstract readReview
In one paragraph

Review in FEBS letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% 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

185 citing papers in PubMed, 1 synthesis or guideline pooled it, 319 citations in OpenAlex.

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125 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 3 countries.

Inhae KangDepartment of Food Science and Nutrition, Jeju National University, Korea.
Charleen T ChuDepartment of Pathology, Center for Neuroscience, Pittsburgh Institute for Neurodegenerative Diseases, Conformational Protein Diseases Center, McGowan Institute for Regenerative Medicine, University of Pittsburgh, PA, USA.
Brett A KaufmanDivision of Cardiology, Department of Medicine, Center for Metabolic and Mitochondrial Medicine (C3M), Vascular Medicine Institute, University of Pittsburgh School of Medicine, PA, USA.
McGowan Institute for Regenerative Medicine · USMRC Mitochondrial Biology Unit · GBUniversity of Pittsburgh · US

Funding

Measuring the Temporal-Spatial Responses of Dormancy and Drug Resistance in a Human Breast Cancer Metastatic Niche within a Liver-on-a-Chip Microphysiological PlatformUH3TR000503 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TAYLOR, D. LANSING · 2014 to 2016
$6.2M
Regulation of Autophagy & Mitochondrial Recycling in Neuronal Cell Death- SupplementR01AG026389 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2007 to 2024
$6.0M
Dendrite regulation by the mitochondrial kinase PINK1: Implications for PD/LBD Diversity SupplementR01NS101628 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Charleen T Chu, Zachary P Wills · 2017 to 2026
$4.0M
Collaborations to Extend the Microphysiology Database for Multiple Organ Models,UH2TR000503 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TAYLOR, D. LANSING, YARMUSH, MARTIN L · 2012 to 2013
$2.3M
Molecular mechanisms of mitochondrial DNA deletion formationR01GM110424 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAUFMAN, BRETT A · 2015 to 2019
$1.9M
PINK1 Regulation of Neuronal and Mitochondrial HomeostasisR01NS065789 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2011 to 2014
$1.3M
PINK1 Regulation of Neuronal and Mitochondrial HomeostasisR56NS065789 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2010 to 2016
$813k
NIA NIH HHS R01 AG026389NIGMS NIH HHS R01 GM110424NINDS NIH HHS R01 NS065789NINDS NIH HHS R01 NS101628NINDS NIH HHS R56 NS065789
6 · The paper itself

Abstract

The mitochondrial transcription factor A, or TFAM, is a mitochondrial DNA (mtDNA)-binding protein essential for genome maintenance. TFAM functions in determining the abundance of the mitochondrial genome by regulating packaging, stability, and replication. More recently, TFAM has been shown to play a central role in the mtDNA stress-mediated inflammatory response. Emerging evidence indicates that decreased mtDNA copy number is associated with several aging-related pathologies; however, little is known about the association of TFAM abundance and disease. In this Review, we evaluate the potential associations of altered TFAM levels or mtDNA copy number with neurodegeneration. We also describe potential mechanisms by which mtDNA replication, transcription initiation, and TFAM-mediated endogenous danger signals may impact mitochondrial homeostasis in Alzheimer, Huntington, Parkinson, and other neurodegenerative diseases.

Indexed as

DNA ReplicationSignal TransductionTranscription Initiation, GeneticAnimalsDNA-Binding ProteinsDNA Copy Number VariationsDNA, MitochondrialGenome, MitochondrialHumansInflammationMitochondrial ProteinsNeurodegenerative DiseasesTranscription FactorsDNA-Binding ProteinsDNA, MitochondrialMitochondrial ProteinsTFAM protein, humanTranscription Factorsmitochondrial DNAneurodegenerationTFAM

Identifiers

PMID29364506
PMCPMC5851836
OpenAlexW2790688909

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.