Evidence map›Paper›PMID 25553274›Full record

ReviewAnnals of laboratory medicine2015

Mitochondrial DNA aberrations and pathophysiological implications in hematopoietic diseases, chronic inflammatory diseases, and cancers.

Hye-Ran Kim, Stephanie Jane Won, Claire Fabian, Min-Gu Kang, Michael Szardenings, Myung-Geun Shin

Abstract readReview
In one paragraph

Review in Annals of laboratory medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

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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

6 authors.

Hye-Ran KimDepartment of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, Hwasun, Korea. ; Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, Korea.
Stephanie Jane WonDepartment of Integrative Biology, University of California, Berkeley, CA, USA.
Claire FabianDepartment of Cell Therapy, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Min-Gu KangDepartment of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, Hwasun, Korea. ; Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, Korea.
Michael SzardeningsDepartment of Cell Therapy, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Myung-Geun ShinDepartment of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, Hwasun, Korea. ; Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, Korea. ; Environment Health Center for Childhood Leukemia and Cancer, Chonnam National University Hwasun Hospital, Hwasun, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are important intracellular organelles that produce energy for cellular development, differentiation, and growth. Mitochondrial DNA (mtDNA) presents a 10- to 20-fold higher susceptibility to genetic mutations owing to the lack of introns and histone proteins. The mtDNA repair system is relatively inefficient, rendering it vulnerable to reactive oxygen species (ROS) produced during ATP synthesis within the mitochondria, which can then target the mtDNA. Under conditions of chronic inflammation and excess stress, increased ROS production can overwhelm the antioxidant system, resulting in mtDNA damage. This paper reviews recent literature describing the pathophysiological implications of oxidative stress, mitochondrial dysfunction, and mitochondrial genome aberrations in aging hematopoietic stem cells, bone marrow failure syndromes, hematological malignancies, solid organ cancers, chronic inflammatory diseases, and other diseases caused by exposure to environmental hazards.

Indexed as

InflammationDNA, MitochondrialHematologic DiseasesHumansMitochondriaMutationNeoplasmsOxidative StressReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen SpeciesAberrationsDiseasesmtDNA

Identifiers

PMID25553274
PMCPMC4272938

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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.