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Bioactive Compounds in the Pathogenesis, Prevention, and Therapy of Eye Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 5601

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Special Issue Information

Dear Colleagues,

Bioactive compounds derived from natural products include a diverse class of compounds with different chemical structures comprising polyphenols, carotenoids, tocopherols, phytosterols, organosulfur compounds, and other classes. While many of them are not essential, their substantial proportion may modulate a number of processes ongoing in our body and are useful in the prevention and therapy of various human disorders. Although several bioactive compounds are reported to have a beneficial effect on vision, the results of clinical trials and systematic reviews on their efficacy in various eye diseases are not conclusive. Therefore, studies on the effects of bioactive compounds in eye diseases are needed and should primarily focus on the involvement of bioactive compounds in pathogenesis mechanisms and preventive and therapeutic potential.

This Special Issue welcomes both original papers and reviews addressing the potential of bioactive compounds in eye disease pathogenesis, prevention, and therapy. The following diseases may be addressed: refractive disorders, dry eye syndrome, cornea degenerations and dystrophies, conjunctiva disorders, cataracts, uveitis, glaucoma, age-related macular degeneration, diabetic retinopathy, albinism, retinopathy of prematurity, retinitis pigmentosa, ocular tumors, lysosomal storage diseases, and rare ophthalmic genetic diseases, as well as chemical and physical damage of the eye studied in cell cultures, animal models, or human material. The following keywords may be useful in selecting a paper topic.

Keywords (all in relation to bioactive compounds in eye diseases):

  • Pathogenesis, prevention, and therapy
  • Bioavailability
  • Genetic/epigenetic
  • Oxidative stress and antioxidant system
  • Stress response
  • Molecular chaperones
  • Senescence and organismal aging
  • Mitochondrial quality control
  • Autophagy and mitophagy
  • DNA damage reaction in the nucleus and mitochondria
  • DNA damage and repair
  • Mutations/polymorphisms of genes
  • Programmed cell death, including apoptosis, pyroptosis, and necroptosis
  • Inflammation and the inflammasome activation
  • miRNA-lncRNA regulation

Prof. Dr. Kai Kaarniranta
Prof. Dr. Janusz Blasiak
Guest Editors

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Research

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12 pages, 6670 KiB  
Article
5-ALA/SFC Ameliorates Endotoxin-Induced Ocular Inflammation in Rats by Inhibiting the NF-κB Signaling Pathway and Activating the HO-1/Nrf2 Signaling Pathway
by Yuya Otaka, Kazutaka Kanai, Arisa Mori, Daiki Okada, Noriaki Nagai, Yohei Yamashita, Yoichiro Ichikawa and Kazuki Tajima
Int. J. Mol. Sci. 2023, 24(10), 8653; https://doi.org/10.3390/ijms24108653 - 12 May 2023
Cited by 2 | Viewed by 1909
Abstract
Sodium ferrous citrate (SFC) is involved in the metabolism of 5-aminolevulinic acid (5-ALA) and enhances its anti-inflammatory effects. The effects of 5-ALA/SFC on inflammation in rats with endotoxin-induced uveitis (EIU) have yet to be elucidated. In this study, during lipopolysaccharide injection, 5-ALA/SFC (10 [...] Read more.
Sodium ferrous citrate (SFC) is involved in the metabolism of 5-aminolevulinic acid (5-ALA) and enhances its anti-inflammatory effects. The effects of 5-ALA/SFC on inflammation in rats with endotoxin-induced uveitis (EIU) have yet to be elucidated. In this study, during lipopolysaccharide injection, 5-ALA/SFC (10 mg/kg 5-ALA plus 15.7 mg/kg SFC) or 5-ALA (10 or 100 mg/kg) was administered via gastric gavage, wherein we saw that 5-ALA/SFC ameliorated ocular inflammation in EIU rats by suppressing clinical scores; by infiltrating cell counts, aqueous humor protein, and inflammatory cytokine levels; and by improving histopathological scores to the same extent as 100 mg/kg 5-ALA. Immunohistochemistry showed that 5-ALA/SFC suppressed iNOS and COX-2 expression, NF-κB activation, IκB-α degradation, and p-IKKα/β expression, and activated HO-1 and Nrf2 expression. Therefore, this study has investigated how 5-ALA/SFC reduces inflammation and revealed the pathways involved in EIU rats. 5-ALA/SFC is shown to inhibit ocular inflammation in EIU rats by inhibiting NF-κB and activating the HO-1/Nrf2 pathways. Full article
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Review

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12 pages, 1550 KiB  
Review
The Role of Ectodysplasin A on the Ocular Surface Homeostasis
by Shangkun Ou, Mani Vimalin Jeyalatha, Yi Mao, Junqi Wang, Chao Chen, Minjie Zhang, Xiaodong Liu, Minghui Liang, Sijie Lin, Yiming Wu, Yixuan Li and Wei Li
Int. J. Mol. Sci. 2022, 23(24), 15700; https://doi.org/10.3390/ijms232415700 - 10 Dec 2022
Cited by 4 | Viewed by 2906
Abstract
Ectodysplasin A (EDA), a ligand of the TNF family, plays an important role in maintaining the homeostasis of the ocular surface. EDA is necessary for the development of the meibomian gland, the lacrimal gland, as well as the proliferation and barrier function of [...] Read more.
Ectodysplasin A (EDA), a ligand of the TNF family, plays an important role in maintaining the homeostasis of the ocular surface. EDA is necessary for the development of the meibomian gland, the lacrimal gland, as well as the proliferation and barrier function of the corneal epithelium. The mutation of EDA can induce the destruction of the ocular surface resulting in keratopathy, abnormality of the meibomian gland and maturation of the lacrimal gland. Experimental animal studies showed that a prenatal ultrasound-guided intra-amniotic injection or postnatal intravenous administration of soluble recombinant EDA protein can efficiently prevent the development of ocular surface abnormalities in EDA mutant animals. Furthermore, local application of EDA could restore the damaged ocular surface to some extent. Hence, a recombinant EDA-based therapy may serve as a novel paradigm to treat ocular surface disorders, such as meibomian gland dysfunction and corneal epithelium abnormalities. Full article
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