SHYAMSUNDER, Pavithra, Milan EŠNER, Maunish BARVALIA, Yu Jun WU, Tomáš LOJA, Huat Bay BOON, Matilde E. LLEONART, Rama S VERMA, Lumír KREJČÍ and Alex LYAKHOVICH. Impaired mitophagy in Fanconi anemia is dependent on mitochondrial fission. Oncotarget. New York: Impact Journals, 2016, vol. 7, No 36, p. 58065-58074. ISSN 1949-2553. Available from: https://dx.doi.org/10.18632/oncotarget.11161.
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Basic information
Original name Impaired mitophagy in Fanconi anemia is dependent on mitochondrial fission
Authors SHYAMSUNDER, Pavithra (702 Singapore), Milan EŠNER (203 Czech Republic, belonging to the institution), Maunish BARVALIA (356 India), Yu Jun WU (702 Singapore), Tomáš LOJA (703 Slovakia, belonging to the institution), Huat Bay BOON (702 Singapore), Matilde E. LLEONART (724 Spain), Rama S VERMA (356 India), Lumír KREJČÍ (203 Czech Republic, guarantor, belonging to the institution) and Alex LYAKHOVICH (643 Russian Federation, belonging to the institution).
Edition Oncotarget, New York, Impact Journals, 2016, 1949-2553.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 5.168
RIV identification code RIV/00216224:14110/16:00091248
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.18632/oncotarget.11161
UT WoS 000387153200048
Keywords in English mitophagy; impaired autophagy; Fanconi anemia; ROS; oxidative stress
Tags EL OK, podil
Tags International impact, Reviewed
Changed by Changed by: Ing. Mgr. Věra Pospíšilíková, učo 9005. Changed: 9/1/2017 14:30.
Abstract
Fanconi anemia (FA) is a rare genetic disorder associated with bone-marrow failure, genome instability and cancer predisposition. Recently, we and others have demonstrated dysfunctional mitochondria with morphological alterations in FA cells accompanied by high reactive oxygen species (ROS) levels. Mitochondrial morphology is regulated by continuous fusion and fission events and the misbalance between these two is often accompanied by autophagy. Here, we provide evidence of impaired autophagy in FA. We demonstrate that FA cells have increased number of autophagic (presumably mitophagic) events and accumulate dysfunctional mitochondria due to an impaired ability to degrade them. Moreover, mitochondrial fission accompanied by oxidative stress (OS) is a prerequisite condition for mitophagy in FA and blocking this pathway may release autophagic machinery to clear dysfunctional mitochondria.
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