Evidence map›Paper›PMID 18458094›Full record

ArticleThe American journal of pathology2008

Expression and maintenance of mitochondrial DNA: new insights into human disease pathology.

Gerald S Shadel

Open access · bronzeAbstract readLecture
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Review
  6. The Evaluation of Mass/DNA Copy Number of Mitochondria in Umbilical Cord Blood-derived Hematopoietic Stem Cells Cocultured with MSCs.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024
    Article
  7. Aging, Cancer, and Inflammation: The Telomerase Connection.International journal of molecular sciences · 2024
    Review
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13 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

1 author at 1 institution in 1 country.

Gerald S ShadelDepartments of Pathology and Genetics, Yale University School of Medicine, 310 Cedar St., P.O. Box 208023, New Haven, CT 06520-8023. gerald.shadel@yale.edu
Yale University · US

Funding

Resistance to UV Damage: Role of Gene RegulationP01ES011163 · NIEHS · EMORY UNIVERSITY · PI DOETSCH, PAUL WILLIAM · 2002 to 2012
$12.6M
Nuclear Control of Mitochondrial Gene ExpressionR01HL059655 · NHLBI · YALE UNIVERSITY · PI SHADEL, GERALD · 1997 to 2011
$3.1M
Mitochondrial Dysfunction and Oxidative Stress in Ataxia TelangiectasiaR01NS056206 · NINDS · YALE UNIVERSITY · PI SHADEL, GERALD · 2007 to 2011
$1.9M
NHLBI NIH HHS HL-059655NHLBI NIH HHS R01 HL059655NIEHS NIH HHS ES-011163NIEHS NIH HHS P01 ES011163NINDS NIH HHS NS-056206NINDS NIH HHS R01 NS056206
6 · The paper itself

Abstract

Mitochondria are central players in cellular energy metabolism and, consequently, defects in their function result in many characterized metabolic diseases. Critical for their function is mitochondrial DNA (mtDNA), which encodes subunits of the oxidative phosphorylation complexes essential for cellular respiration and ATP production. Expression, replication, and maintenance of mtDNA require factors encoded by nuclear genes. These include not only the primary machinery involved (eg, transcription and replication components) but also those in signaling pathways that mediate or sense alterations in mitochondrial function in accord with changing cellular needs or environmental conditions. Mutations in these contribute to human disease pathology by mechanisms that are being revealed at an unprecedented rate. As I will discuss herein, the basic protein machinery required for transcription initiation in human mitochondria has been elucidated after the discovery of two multifunctional mitochondrial transcription factors, h-mtTFB1 and h-mtTFB2, that are also rRNA methyltransferases. In addition, involvement of the ataxia-telangiectasia mutated (ATM) and target of rapamycin (TOR) signaling pathways in regulating mitochondrial homeostasis and gene expression has also recently been uncovered. These advancements embody the current mitochondrial research landscape, which can be described as exploding with discoveries of previously unanticipated roles for mitochondria in human disease and aging.

Indexed as

AgingAnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA, MitochondrialGene Expression RegulationHumansMethyltransferasesMitochondrial DiseasesMitochondrial ProteinsMutationPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)Protein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsDNA, MitochondrialMethyltransferasesMitochondrial ProteinsPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)Protein Serine-Threonine KinasesrRNA (adenosine-O-2'-)methyltransferaseSaccharomyces cerevisiae ProteinsTFB1M protein, humanTFB2M protein, humanTOR1 protein, S cerevisiaeTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID18458094
PMCPMC2408405
OpenAlexW1774344187

What OpenQuestion holds

Textmetadata
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.