PMID- 33670885
OWN - NLM
STAT- MEDLINE
DCOM- 20210430
LR  - 20231111
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 22
IP  - 5
DP  - 2021 Feb 28
TI  - Crosstalk between MicroRNA and Oxidative Stress in Primary Open-Angle Glaucoma.
LID - 10.3390/ijms22052421 [doi]
LID - 2421
AB  - Reactive oxygen species (ROS) plays a key role in the pathogenesis of primary 
      open-angle glaucoma (POAG), a chronic neurodegenerative disease that damages the 
      trabecular meshwork (TM) cells, inducing apoptosis of the retinal ganglion cells 
      (RGC), deteriorating the optic nerve head, and leading to blindness. Aqueous 
      humor (AH) outflow resistance and intraocular pressure (IOP) elevation contribute 
      to disease progression. Nevertheless, despite the existence of pharmacological 
      and surgical treatments, there is room for the development of additional 
      treatment approaches. The following review is aimed at investigating the role of 
      different microRNAs (miRNAs) in the expression of genes and proteins involved in 
      the regulation of inflammatory and degenerative processes, focusing on the 
      delicate balance of synthesis and deposition of extracellular matrix (ECM) 
      regulated by chronic oxidative stress in POAG related tissues. The neutralizing 
      activity of a couple of miRNAs was described, suggesting effective downregulation 
      of pro-inflammatory and pro-fibrotic signaling pathways, including nuclear factor 
      kappa-light-chain-enhancer of activated B cells (NF-kB), transforming growth 
      factor-beta 2 (TGF-beta2), Wnt/beta-Catenin, and PI3K/AKT. In addition, with regards to 
      the elevated IOP in many POAG patients due to increased outflow resistance, 
      Collagen type I degradation was stimulated by some miRNAs and prevented ECM 
      deposition in TM cells. Mitochondrial dysfunction as a consequence of oxidative 
      stress was suppressed following exposure to different miRNAs. In contrast, 
      increased oxidative damage by inhibiting the mTOR signaling pathway was described 
      as part of the action of selected miRNAs. Summarizing, specific miRNAs may be 
      promising therapeutic targets for lowering or preventing oxidative stress injury 
      in POAG patients.
FAU - Tabak, Saray
AU  - Tabak S
AD  - Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of 
      the Negev, Beer-Sheva 84105, Israel.
FAU - Schreiber-Avissar, Sofia
AU  - Schreiber-Avissar S
AD  - Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of 
      the Negev, Beer-Sheva 84105, Israel.
FAU - Beit-Yannai, Elie
AU  - Beit-Yannai E
AUID- ORCID: 0000-0001-9347-822X
AD  - Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of 
      the Negev, Beer-Sheva 84105, Israel.
LA  - eng
GR  - 1545/20/Israel Science Foundation/
PT  - Journal Article
PT  - Review
DEP - 20210228
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - *Aqueous Humor
MH  - Glaucoma, Open-Angle/*metabolism/physiopathology
MH  - Humans
MH  - Intraocular Pressure
MH  - MicroRNAs/*metabolism
MH  - *Oxidative Stress
MH  - Signal Transduction
MH  - Trabecular Meshwork/*metabolism/physiopathology
PMC - PMC7957693
OTO - NOTNLM
OT  - aqueous humor
OT  - intraocular pressure
OT  - miRNA
OT  - oxidative stress
OT  - primary open angle glaucoma
OT  - retinal ganglion cells
OT  - trabecular meshwork
COIS- The authors declare no conflict of interest.
EDAT- 2021/03/07 06:00
MHDA- 2021/05/01 06:00
PMCR- 2021/02/28
CRDT- 2021/03/06 01:08
PHST- 2021/01/25 00:00 [received]
PHST- 2021/02/23 00:00 [revised]
PHST- 2021/02/24 00:00 [accepted]
PHST- 2021/03/06 01:08 [entrez]
PHST- 2021/03/07 06:00 [pubmed]
PHST- 2021/05/01 06:00 [medline]
PHST- 2021/02/28 00:00 [pmc-release]
AID - ijms22052421 [pii]
AID - ijms-22-02421 [pii]
AID - 10.3390/ijms22052421 [doi]
PST - epublish
SO  - Int J Mol Sci. 2021 Feb 28;22(5):2421. doi: 10.3390/ijms22052421.