Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.3
4.1
Journals
Metabolites
Special Issues
Bioenergetics and Cellular Dysfunction in the Brain and Eye
share announcement

Bioenergetics and Cellular Dysfunction in the Brain and Eye

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 10160

Special Issue Editors

Dr. Tina McKay

E-Mail Website
Guest Editor
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA
Interests: biomarkers; delirium; cornea; cellular metabolism; extracellular matrix
Dr. Daisy Y. Shu

E-Mail Website
Guest Editor
Department of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, Harvard Medical School, Boston, MA 02114, USA
Interests: epithelial-mesenchymal transition; metabolism; mitochondria; growth factors; signalling pathways

Special Issue Information

Dear Colleagues,

Given their high metabolic requirements, the brain and retina are particularly susceptible to deficits in nutrition and oxygen availability. Both mitochondrial dysfunction and increased oxidative stress are common traits shared in neurodegenerative diseases, such as Alzheimer’s disease and age-related macular degeneration. In recent years, the role for oxidative stress in diseases of the cornea, including keratoconus and Fuchs corneal endothelial disease, has also been reported.

This Special Issue is focused on studies evaluating cellular metabolism during physiological and pathological conditions with emphasis on the brain and eye, as model tissues for the study of bioenergetics and oxidative stress. All papers related to investigations of metabolite biomarkers, metabolic networks, and mitochondrial function are welcome. Specific topics include, but are not limited to, Alzheimer’s disease and related dementias, delirium, keratoconus, Fuchs corneal endothelial disease, age-related macular degeneration, diabetes, mitochondrial disorders, and cellular or systemic biomarkers of oxidative stress. Review articles covering these topics are also invited.

Dr. Tina B. McKay
Dr. Daisy Y. Shu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • brain metabolism
  • delirium
  • Alzheimer’s disease and related dementias
  • cornea
  • keratoconus
  • diabetes
  • mitochondrial dysfunction
  • oxidatve stress
  • metabolomics
  • aging
  • proteomics
  • transcriptomics
  • tissue-engineered models

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 2674 KiB  
Article
Divergent Metabolomic Signatures of TGFβ2 and TNFα in the Induction of Retinal Epithelial-Mesenchymal Transition
by Pei Qin Ng, Magali Saint-Geniez, Leo A. Kim and Daisy Y. Shu
Metabolites 2023, 13(2), 213; https://doi.org/10.3390/metabo13020213 - 31 Jan 2023
Cited by 1 | Viewed by 3756
Abstract
Epithelial-mesenchymal transition (EMT) is a dedifferentiation program in which polarized, differentiated epithelial cells lose their cell-cell adhesions and transform into matrix-producing mesenchymal cells. EMT of retinal pigment epithelial (RPE) cells plays a crucial role in many retinal diseases, including age-related macular degeneration, proliferative [...] Read more.
Epithelial-mesenchymal transition (EMT) is a dedifferentiation program in which polarized, differentiated epithelial cells lose their cell-cell adhesions and transform into matrix-producing mesenchymal cells. EMT of retinal pigment epithelial (RPE) cells plays a crucial role in many retinal diseases, including age-related macular degeneration, proliferative vitreoretinopathy, and diabetic retinopathy. This dynamic process requires complex metabolic reprogramming to accommodate the demands of this dramatic cellular transformation. Both transforming growth factor-beta 2 (TGFβ2) and tumor necrosis factor-alpha (TNFα) have the capacity to induce EMT in RPE cells; however, little is known about their impact on the RPE metabolome. Untargeted metabolomics using high-resolution mass spectrometry was performed to reveal the metabolomic signatures of cellular and secreted metabolites of primary human fetal RPE cells treated with either TGFβ2 or TNFα for 5 days. A total of 638 metabolites were detected in both samples; 188 were annotated as primary metabolites. Metabolomics profiling showed distinct metabolomic signatures associated with TGFβ2 and TNFα treatment. Enrichment pathway network analysis revealed alterations in the pentose phosphate pathway, galactose metabolism, nucleotide and pyrimidine metabolism, purine metabolism, and arginine and proline metabolism in TNFα-treated cells compared to untreated control cells, whereas TGFβ2 treatment induced perturbations in fatty acid biosynthesis metabolism, the linoleic acid pathway, and the Notch signaling pathway. These results provide a broad metabolic understanding of the bioenergetic rewiring processes governing TGFβ2- and TNFα-dependent induction of EMT. Elucidating the contributions of TGFβ2 and TNFα and their mechanistic differences in promoting EMT of RPE will enable the identification of novel biomarkers for diagnosis, management, and tailored drug development for retinal fibrotic diseases. Full article
(This article belongs to the Special Issue Bioenergetics and Cellular Dysfunction in the Brain and Eye)
►▼ Show Figures

Graphical abstract

11 pages, 2381 KiB  
Article
Quercetin Decreases Corneal Haze In Vivo and Influences Gene Expression of TGF-Beta Mediators In Vitro
by Tina B. McKay, Pouriska B. Kivanany, Sarah E. Nicholas, Okhil K. Nag, Michael H. Elliott, W. Matthew Petroll and Dimitrios Karamichos
Metabolites 2022, 12(7), 626; https://doi.org/10.3390/metabo12070626 - 07 Jul 2022
Cited by 5 | Viewed by 1620
Abstract
We have previously reported the flavonoid, quercetin, as a metabolic regulator and inhibitor of myofibroblast differentiation in vitro. Our current study evaluated the effects of topical application of quercetin on corneal scar development using two different animal models followed by RNA analysis in [...] Read more.
We have previously reported the flavonoid, quercetin, as a metabolic regulator and inhibitor of myofibroblast differentiation in vitro. Our current study evaluated the effects of topical application of quercetin on corneal scar development using two different animal models followed by RNA analysis in vitro. Wild-type C57BL/6J mice were anesthetized and the corneal epithelium and stroma were manually debrided, followed by quercetin (0.5, 1, 5, or 50 mM) or vehicle application. Corneal scarring was assessed for 3 weeks by slit lamp imaging and clinically scored. In a separate animal study, six New Zealand White rabbits underwent lamellar keratectomy surgery, followed by treatment with 5 mM quercetin or vehicle twice daily for three days. Stromal backscattering was assessed at week 3 by in vivo confocal microscopy. In mice, a single dose of 5 mM quercetin reduced corneal scar formation. In rabbits, stromal backscattering was substantially lower in two out of three animals in the quercetin-treated group. In vitro studies of human corneal fibroblasts showed that quercetin modulated select factors of the transforming growth factor-β (TGF-β) signaling pathway. These results provide evidence that quercetin may inhibit corneal scarring. Further studies in a larger cohort are required to validate the efficacy and safety of quercetin for clinical applications. Full article
(This article belongs to the Special Issue Bioenergetics and Cellular Dysfunction in the Brain and Eye)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

40 pages, 1804 KiB  
Review
Role of Oxidative Stress in Ocular Diseases: A Balancing Act
by Daisy Y. Shu, Suman Chaudhary, Kin-Sang Cho, Anton Lennikov, William P. Miller, David C. Thorn, Menglu Yang and Tina B. McKay
Metabolites 2023, 13(2), 187; https://doi.org/10.3390/metabo13020187 - 27 Jan 2023
Cited by 17 | Viewed by 3783
Abstract
Redox homeostasis is a delicate balancing act of maintaining appropriate levels of antioxidant defense mechanisms and reactive oxidizing oxygen and nitrogen species. Any disruption of this balance leads to oxidative stress, which is a key pathogenic factor in several ocular diseases. In this [...] Read more.
Redox homeostasis is a delicate balancing act of maintaining appropriate levels of antioxidant defense mechanisms and reactive oxidizing oxygen and nitrogen species. Any disruption of this balance leads to oxidative stress, which is a key pathogenic factor in several ocular diseases. In this review, we present the current evidence for oxidative stress and mitochondrial dysfunction in conditions affecting both the anterior segment (e.g., dry eye disease, keratoconus, cataract) and posterior segment (age-related macular degeneration, proliferative vitreoretinopathy, diabetic retinopathy, glaucoma) of the human eye. We posit that further development of therapeutic interventions to promote pro-regenerative responses and maintenance of the redox balance may delay or prevent the progression of these major ocular pathologies. Continued efforts in this field will not only yield a better understanding of the molecular mechanisms underlying the pathogenesis of ocular diseases but also enable the identification of novel druggable redox targets and antioxidant therapies. Full article
(This article belongs to the Special Issue Bioenergetics and Cellular Dysfunction in the Brain and Eye)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop