نتایج جستجو برای: mitochondrial damage

تعداد نتایج: 349971  

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1997
F M Yakes B Van Houten

A significant amount of reactive oxygen species (ROS) is generated during mitochondrial oxidative phosphorylation. Several studies have suggested that mtDNA may accumulate more oxidative DNA damage relative to nuclear DNA. This study used quantitative PCR to examine the formation and repair of hydrogen peroxide-induced DNA damage in a 16.2-kb mitochondrial fragment and a 17.7-kb fragment flanki...

Journal: :Circulation 2014
Wai Ho Tang Jeremiah Stitham Yu Jin Renjing Liu Seung Hee Lee Jing Du Gourg Atteya Scott Gleim Geralyn Spollett Kathleen Martin John Hwa

BACKGROUND Platelet abnormalities are well-recognized complications of diabetes mellitus. Mitochondria play a central role in platelet metabolism and activation. Mitochondrial dysfunction is evident in diabetes mellitus. The molecular pathway for hyperglycemia-induced mitochondrial dysfunction in platelets in diabetes mellitus is unknown. METHODS AND RESULTS Using both human and humanized mou...

2017
Song-Yun Deng Le-Meng Zhang Yu-hang Ai Pin-Hua Pan Shuang-Ping Zhao Xiao-Li Su Dong-Dong Wu Hong-Yi Tan Li-Na Zhang Allan Tsung

Sepsis causes many early deaths; both macrophage mitochondrial damage and oxidative stress responses are key factors in its pathogenesis. Although the exact mechanisms responsible for sepsis-induced mitochondrial damage are unknown, the nuclear transcription factor, interferon regulatory factor-1 (IRF-1) has been reported to cause mitochondrial damage in several diseases. Previously, we reporte...

Ataxia-Telangiectasia (AT) is a rare human neurodegenerative autosomal recessive multisystem disease that is characterized by a wide range of features including, progressive cerebellar ataxia with onset during infancy, occulocutaneous telangiectasia, susceptibility to neoplasia, occulomotor disturbances, chromosomal instability and growth and developmental abnormalities. Mitochondrial DNA (mtDN...

Journal: :genetics in the 3rd millennium 0
محمد مهدی بانویی mohammad mehdi banoei national institute for genetic engineering and biotechnology, tehran, iran مسعود هوشمند massoud houshmand national institute for genetic engineering and biotechnology, tehran, iran مهدی شریعت پناهی mehdi shafa shariatpanahi national institute for genetic engineering and biotechnology, tehran, iran پروین شریعتی parvin shariati national institute for genetic engineering and biotechnology, tehran, iran مریم رستمی maryam rostami national institute for genetic engineering and biotechnology, tehran, iran معصومه دهقان منشدی masoumeh dehghan manshadi national institute for genetic engineering and biotechnology, tehran, iran طیبه مجیدی زاده

the mitochondrial dna (mtdna) may play an essential role in the pathogenesis of the respiratory chain complex activities in neurodegenerative disorders such as huntington’s disease (hd). research studies have been conducted to determine the possible levels of mitochondrial defect (deletion) in hd patients and the interaction between the expanded huntingtin gene as a nuclear gene and mitochondri...

B-acute lymphoblastic leukemia (B-ALL) is the frequent pediatric malignity. Chemotherapy is the most practical approaches to deal with such malignancies. Microtubule-targeted agents are one of the most strategic drugs which formerly use in chemotherapy.Although,colchicine-binding anti-tubulin agents exhibited promising effects in clinical trials, their exact mechanism of action is not fully und...

Journal: :Chinese Medical Journal 2018

Journal: :Journal of Radiation Research 2014

2017
Emma P.K. Yu Johannes Reinhold Haixiang Yu Lakshi Starks Anna K. Uryga Kirsty Foote Alison Finigan Nichola Figg Yuh-Fen Pung Angela Logan Michael P. Murphy Martin Bennett

OBJECTIVE Mitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction and whether decreasing mtDNA damage and improving mitochondrial respiration affects plaque burden or composition are unclear. We examined mitochondrial respiration in human atherosclerotic plaques ...

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