PMID- 31091656
OWN - NLM
STAT- MEDLINE
DCOM- 20190826
LR  - 20200225
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 20
IP  - 10
DP  - 2019 May 14
TI  - Role of Mitochondrial DNA Damage in ROS-Mediated Pathogenesis of Age-Related 
      Macular Degeneration (AMD).
LID - 10.3390/ijms20102374 [doi]
LID - 2374
AB  - Age-related macular degeneration (AMD) is a complex eye disease that affects 
      millions of people worldwide and is the main reason for legal blindness and 
      vision loss in the elderly in developed countries. Although the cause of AMD 
      pathogenesis is not known, oxidative stress-related damage to retinal pigment 
      epithelium (RPE) is considered an early event in AMD induction. However, the 
      precise cause of such damage and of the induction of oxidative stress, including 
      related oxidative effects occurring in RPE and the onset and progression of AMD, 
      are not well understood. Many results point to mitochondria as a source of 
      elevated levels of reactive oxygen species (ROS) in AMD. This ROS increase can be 
      associated with aging and effects induced by other AMD risk factors and is 
      correlated with damage to mitochondrial DNA. Therefore, mitochondrial DNA (mtDNA) 
      damage can be an essential element of AMD pathogenesis. This is supported by many 
      studies that show a greater susceptibility of mtDNA than nuclear DNA to 
      DNA-damaging agents in AMD. Therefore, the mitochondrial DNA damage reaction 
      (mtDDR) is important in AMD prevention and in slowing down its progression as is 
      ROS-targeting AMD therapy. However, we know far less about mtDNA than its nuclear 
      counterparts. Further research should measure DNA damage in order to compare it 
      in mitochondria and the nucleus, as current methods have serious disadvantages.
FAU - Kaarniranta, Kai
AU  - Kaarniranta K
AUID- ORCID: 0000-0003-2600-8679
AD  - Department of Ophthalmology, University of Eastern Finland, 70211 Kuopio, 
      Finland. kai.kaarniranta@kuh.fi.
AD  - Department of Ophthalmology, Kuopio University Hospital, 70029 Kuopio, Finland. 
      kai.kaarniranta@kuh.fi.
FAU - Pawlowska, Elzbieta
AU  - Pawlowska E
AD  - Department of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland. 
      elzbieta.pawlowska@umed.lodz.pl.
FAU - Szczepanska, Joanna
AU  - Szczepanska J
AD  - Department of Pediatric Dentistry, Medical University of Lodz, 92-216 Lodz, 
      Poland. joanna.szczepanska@umed.lodz.pl.
FAU - Jablkowska, Aleksandra
AU  - Jablkowska A
AUID- ORCID: 0000-0001-9854-5233
AD  - Department of Infectious and Liver Diseases, W. Bieganski Hospital, 91-347 Lodz, 
      Poland. jablkowska@pro.onet.pl.
FAU - Blasiak, Janusz
AU  - Blasiak J
AUID- ORCID: 0000-0001-9539-9584
AD  - Department of Molecular Genetics, Faculty of Biology and Environmental 
      Protection, University of Lodz, 90-236 Lodz, Poland. 
      janusz.blasiak@biol.uni.lodz.pl.
LA  - eng
GR  - 2017/27/B/NZ3/00872/National Science Centre, Poland/
PT  - Journal Article
PT  - Review
DEP - 20190514
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (Reactive Oxygen Species)
MH  - Animals
MH  - *DNA Damage
MH  - DNA, Mitochondrial/*genetics
MH  - Humans
MH  - Macular Degeneration/*etiology
MH  - Reactive Oxygen Species/*metabolism
PMC - PMC6566654
OTO - NOTNLM
OT  - DNA damage response
OT  - age-related macular degeneration
OT  - mitochondria
OT  - mtDNA damage
OT  - reactive oxygen species
COIS- The authors declare no conflict of interest.
EDAT- 2019/05/17 06:00
MHDA- 2019/08/27 06:00
PMCR- 2019/05/01
CRDT- 2019/05/17 06:00
PHST- 2019/02/18 00:00 [received]
PHST- 2019/04/17 00:00 [revised]
PHST- 2019/04/28 00:00 [accepted]
PHST- 2019/05/17 06:00 [entrez]
PHST- 2019/05/17 06:00 [pubmed]
PHST- 2019/08/27 06:00 [medline]
PHST- 2019/05/01 00:00 [pmc-release]
AID - ijms20102374 [pii]
AID - ijms-20-02374 [pii]
AID - 10.3390/ijms20102374 [doi]
PST - epublish
SO  - Int J Mol Sci. 2019 May 14;20(10):2374. doi: 10.3390/ijms20102374.