Editorial

Jump to: Research, Review, Other

3 pages, 193 KiB

Open AccessEditorial

New Discoveries in Retinal Cell Degeneration and Retinal Diseases

by Puran S. Bora

Biomolecules 2023, 13(7), 1121; https://doi.org/10.3390/biom13071121 - 14 Jul 2023

Cited by 1 | Viewed by 790

Abstract

Age-related macular degeneration (AMD) has two phenotypes: dry AMD and wet AMD [...] Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

Research

Jump to: Editorial, Review, Other

21 pages, 3232 KiB

Open AccessArticle

Enhanced Biosafety of the Sleeping Beauty Transposon System by Using mRNA as Source of Transposase to Efficiently and Stably Transfect Retinal Pigment Epithelial Cells

by Nina Harmening, Sandra Johnen, Zsuzsanna Izsvák, Zoltan Ivics, Martina Kropp, Thais Bascuas, Peter Walter, Andreas Kreis, Bojan Pajic and Gabriele Thumann

Biomolecules 2023, 13(4), 658; https://doi.org/10.3390/biom13040658 - 07 Apr 2023

Cited by 2 | Viewed by 2122

Abstract

Neovascular age-related macular degeneration (nvAMD) is characterized by choroidal neovascularization (CNV), which leads to retinal pigment epithelial (RPE) cell and photoreceptor degeneration and blindness if untreated. Since blood vessel growth is mediated by endothelial cell growth factors, including vascular endothelial growth factor (VEGF), [...] Read more.

Neovascular age-related macular degeneration (nvAMD) is characterized by choroidal neovascularization (CNV), which leads to retinal pigment epithelial (RPE) cell and photoreceptor degeneration and blindness if untreated. Since blood vessel growth is mediated by endothelial cell growth factors, including vascular endothelial growth factor (VEGF), treatment consists of repeated, often monthly, intravitreal injections of anti-angiogenic biopharmaceuticals. Frequent injections are costly and present logistic difficulties; therefore, our laboratories are developing a cell-based gene therapy based on autologous RPE cells transfected ex vivo with the pigment epithelium derived factor (PEDF), which is the most potent natural antagonist of VEGF. Gene delivery and long-term expression of the transgene are enabled by the use of the non-viral Sleeping Beauty (SB100X) transposon system that is introduced into the cells by electroporation. The transposase may have a cytotoxic effect and a low risk of remobilization of the transposon if supplied in the form of DNA. Here, we investigated the use of the SB100X transposase delivered as mRNA and showed that ARPE-19 cells as well as primary human RPE cells were successfully transfected with the Venus or the PEDF gene, followed by stable transgene expression. In human RPE cells, secretion of recombinant PEDF could be detected in cell culture up to one year. Non-viral ex vivo transfection using SB100X-mRNA in combination with electroporation increases the biosafety of our gene therapeutic approach to treat nvAMD while ensuring high transfection efficiency and long-term transgene expression in RPE cells. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

10 pages, 2304 KiB

Open AccessArticle

Mitochondrial Triglyceride Dysregulation in Optic Nerves Following Indirect Traumatic Optic Neuropathy

by Muhammad Z. Chauhan, Joseph G. Chacko, Alireza Ghaffarieh, Chloe M. Moulin, Daniel Pelaez, Sami H. Uwaydat and Sanjoy K. Bhattacharya

Biomolecules 2022, 12(12), 1885; https://doi.org/10.3390/biom12121885 - 15 Dec 2022

Cited by 1 | Viewed by 1851

Abstract

The purpose of this work is to identify mitochondrial optic nerve (ON) lipid alterations associated with sonication-induced traumatic optic neuropathy (TON). Briefly, a mouse model of indirect TON was generated using sound energy concentrated focally at the entrance of the optic canal using [...] Read more.

The purpose of this work is to identify mitochondrial optic nerve (ON) lipid alterations associated with sonication-induced traumatic optic neuropathy (TON). Briefly, a mouse model of indirect TON was generated using sound energy concentrated focally at the entrance of the optic canal using a laboratory sonifier (Branson Digital Sonifier 450, Danbury, CT, USA) with a microtip probe. We performed an analysis of a previously generated dataset from high-performance liquid chromatography-electrospray tandem mass spectrometry (LC-MS/MS). We analyzed lipids from isolated mitochondria from the ON at 1 day, 7 days, and 14 days post-sonication compared to non-sonicated controls. Lipid abundance alterations in post-sonicated ON mitochondria were evaluated with 1-way ANOVA (FDR-adjusted significant p-value < 0.01), debiased sparse partial correlation (DSPC) network modeling, and partial least squares-discriminant analysis (PLS-DA). We find temporal alterations in triglyceride metabolism are observed in ON mitochondria of mice following sonication-induced optic neuropathy with notable depletions of TG(18:1/18:2/18:2), TG(18:1/18:1/18:1), and TG(16:0/16:0/18:1). Depletion of mitochondrial triglycerides may mediate ON damage in indirect traumatic optic neuropathy through loss energy substrates for neuronal metabolism. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

13 pages, 3535 KiB

Open AccessArticle

Mitochondrial Dysfunction in a High Intraocular Pressure-Induced Retinal Ischemia Minipig Model

by Michael Pasák, Marie Vanišová, Lucie Tichotová, Jana Křížová, Taras Ardan, Yaroslav Nemesh, Jana Čížková, Anastasiia Kolesnikova, Ruslan Nyshchuk, Natasha Josifovska, Lyubomyr Lytvynchuk, Miriam Kolko, Jan Motlík, Goran Petrovski and Hana Hansíková

Biomolecules 2022, 12(10), 1532; https://doi.org/10.3390/biom12101532 - 21 Oct 2022

Cited by 4 | Viewed by 1662

Abstract

Purpose: Retinal ischemia (RI) and progressive neuronal death are sight-threatening conditions. Mitochondrial (mt) dysfunction and fusion/fission processes have been suggested to play a role in the pathophysiology of RI. This study focuses on changes in the mt parameters of the neuroretina, retinal pigment [...] Read more.

Purpose: Retinal ischemia (RI) and progressive neuronal death are sight-threatening conditions. Mitochondrial (mt) dysfunction and fusion/fission processes have been suggested to play a role in the pathophysiology of RI. This study focuses on changes in the mt parameters of the neuroretina, retinal pigment epithelium (RPE) and choroid in a porcine high intraocular pressure (IOP)-induced RI minipig model. Methods: In one eye, an acute IOP elevation was induced in minipigs and compared to the other control eye. Activity and amount of respiratory chain complexes (RCC) were analyzed by spectrophotometry and Western blot, respectively. The coenzyme Q10 (CoQ10) content was measured using HPLC, and the ultrastructure of the mt was studied via transmission electron microscopy. The expression of selected mt-pathway genes was determined by RT-PCR. Results: At a functional level, increased RCC I activity and decreased total CoQ10 content were found in RPE cells. At a protein level, CORE2, a subunit of RCC III, and DRP1, was significantly decreased in the neuroretina. Drp1 and Opa1, protein-encoding genes responsible for mt quality control, were decreased in most of the samples from the RPE and neuroretina. Conclusions: The eyes of the minipig can be considered a potential RI model to study mt dysfunction in this disease. Strategies targeting mt protection may provide a promising way to delay the acute damage and onset of RI. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

29 pages, 5530 KiB

Open AccessArticle

Modeling Reactive Oxygen Species-Induced Axonal Loss in Leber Hereditary Optic Neuropathy

by Darius W. Lambiri and Leonard A. Levin

Biomolecules 2022, 12(10), 1411; https://doi.org/10.3390/biom12101411 - 02 Oct 2022

Cited by 4 | Viewed by 1807

Abstract

Leber hereditary optic neuropathy (LHON) is a rare syndrome that results in vision loss. A necessary but not sufficient condition for its onset is the existence of known mitochondrial DNA mutations that affect complex I biomolecular structure. Cybrids with LHON mutations generate higher [...] Read more.

Leber hereditary optic neuropathy (LHON) is a rare syndrome that results in vision loss. A necessary but not sufficient condition for its onset is the existence of known mitochondrial DNA mutations that affect complex I biomolecular structure. Cybrids with LHON mutations generate higher rates of reactive oxygen species (ROS). This study models how ROS, particularly H₂O₂, could signal and execute the axonal degeneration process that underlies LHON. We modeled and explored several hypotheses regarding the influence of H₂O₂ on the dynamics of propagation of axonal degeneration in LHON. Zonal oxidative stress, corresponding to H₂O₂ gradients, correlated with the morphology of injury exhibited in the LHON pathology. If the axonal membrane is highly permeable to H₂O₂ and oxidative stress induces larger production of H₂O₂, small injuries could trigger cascading failures of neighboring axons. The cellular interdependence created by H₂O₂ diffusion, and the gradients created by tissue variations in H₂O₂ production and scavenging, result in injury patterns and surviving axonal loss distributions similar to LHON tissue samples. Specifically, axonal degeneration starts in the temporal optic nerve, where larger groups of small diameter fibers are located and propagates from that region. These findings correlate well with clinical observations of central loss of visual field, visual acuity, and color vision in LHON, and may serve as an in silico platform for modeling the mechanism of action for new therapeutics. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

16 pages, 9814 KiB

Open AccessFeature PaperArticle

Fibrillin-1 Regulates Arteriole Integrity in the Retina

by Florian Alonso, Ling Li, Isabelle Fremaux, Dieter Peter Reinhardt and Elisabeth Génot

Biomolecules 2022, 12(10), 1330; https://doi.org/10.3390/biom12101330 - 20 Sep 2022

Cited by 5 | Viewed by 2390

Abstract

Fibrillin-1 is an extracellular matrix protein that assembles into microfibrils that provide critical functions in large blood vessels and other tissues. Mutations in the fibrillin-1 gene are associated with cardiovascular, ocular, and skeletal abnormalities in Marfan syndrome. Fibrillin-1 is a component of the [...] Read more.

Fibrillin-1 is an extracellular matrix protein that assembles into microfibrils that provide critical functions in large blood vessels and other tissues. Mutations in the fibrillin-1 gene are associated with cardiovascular, ocular, and skeletal abnormalities in Marfan syndrome. Fibrillin-1 is a component of the wall of large arteries but has been poorly described in other vessels. We examined the microvasculature in the retina using wild type mice and two models of Marfan syndrome, Fbn1^C1041G/+ and Fbn1^mgR/mgR. In the mouse retina, fibrillin-1 was detected around arterioles, in close contact with the basement membrane, where it colocalized with MAGP1. Both a mutation in fibrillin-1 or fibrillin-1 underexpression characteristically altered the microvasculature. In Fbn1^C1041G/+ and Fbn1^mgR/mgR mice, arterioles were enlarged with reduced MAGP1 deposition and focal loss of smooth muscle cell coverage. Losartan, which prevents aortic enlargement in Fbn1^C1041G/+ mice, prevented smooth muscle cell loss and vessel leakiness when administrated in a preventive mode. Moreover, losartan also partially rescued the defects in a curative mode. Thus, fibrillin-1/MAGP1 performs essential functions in arteriolar integrity and mutant fibrillin-1-induced defects can be prevented or partially rescued pharmacologically. These new findings could have implications for people with Marfan syndrome. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Graphical abstract

10 pages, 1490 KiB

Open AccessArticle

Role of Adiponectin Peptide I (APNp1) in Age-Related Macular Degeneration

by Connor Logan, Valeriy Lyzogubov, Nalini Bora and Puran Bora

Biomolecules 2022, 12(9), 1232; https://doi.org/10.3390/biom12091232 - 03 Sep 2022

Cited by 4 | Viewed by 1710

Abstract

Age-related macular degeneration (AMD) is an eye disease that can cause central vision loss, particularly in the elderly population. There are 2 classes of AMD, wet-type and dry-type. Wet-type involves excess angiogenesis around the macula, referred to as choroidal neovascularization (CNV). This can [...] Read more.

Age-related macular degeneration (AMD) is an eye disease that can cause central vision loss, particularly in the elderly population. There are 2 classes of AMD, wet-type and dry-type. Wet-type involves excess angiogenesis around the macula, referred to as choroidal neovascularization (CNV). This can result in leaky vessels, often causing more severe vision loss than dry-type AMD. Adiponectin peptide 1 (APNp1) has been shown to slow the progression of CNV. Here, we used a mouse model and FITC-labeled APNp1 to determine if APNp1 could be delivered effectively as an eye drop. Our experiment revealed that topically applied FITC-APNp1 could reach the macula of the eye, which is crucial for treating wet-type AMD. We also tested delivery of APNp1 via injection of an adeno-associated virus (AAV) vector in a mouse model of CNV. AAV is a harmless virus easy to manipulate and is very often used for protein or peptide deliveries. Results revealed an increase in the expression of APNp1 in the retina and choroid over a 28-day period. Finally, we investigated the mechanism by which APNp1 affects CNV by examining the expression of adiponectin receptor 1 (AdipoR1) and proliferating cell nuclear antigen (PCNA) in the retinal and choroidal tissue of the mouse eyes. AdipoR1 and PCNA were overexpressed in these tissues in mice with laser-induced CNV compared to naïve mice. Based on our data shown here, we think it will enhance our understanding of APNp1 as a therapeutic agent for wet-type AMD and possible treatment alternatives that could be more beneficial for patients. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

Review

Jump to: Editorial, Research, Other

12 pages, 1229 KiB

Open AccessReview

Role of Complement in the Onset of Age-Related Macular Degeneration

by Niloofar Piri and Henry J. Kaplan

Biomolecules 2023, 13(5), 832; https://doi.org/10.3390/biom13050832 - 13 May 2023

Cited by 2 | Viewed by 1575

Abstract

Age-related macular degeneration (AMD) is a progressive degenerative disease of the central retina and the leading cause of severe loss of central vision in people over age 50. Patients gradually lose central visual acuity, compromising their ability to read, write, drive, and recognize [...] Read more.

Age-related macular degeneration (AMD) is a progressive degenerative disease of the central retina and the leading cause of severe loss of central vision in people over age 50. Patients gradually lose central visual acuity, compromising their ability to read, write, drive, and recognize faces, all of which greatly impact daily life activities. Quality of life is significantly affected in these patients, and there are worse levels of depression as a result. AMD is a complex, multifactorial disease in which age and genetics, as well as environmental factors, all play a role in its development and progression. The mechanism by which these risk factors interact and converge towards AMD are not fully understood, and therefore, drug discovery is challenging, with no successful therapeutic attempt to prevent the development of this disease. In this review, we describe the pathophysiology of AMD and review the role of complement, which is a major risk factor in the development of AMD. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

13 pages, 734 KiB

Open AccessReview

The Autoimmune Rheumatic Disease Related Dry Eye and Its Association with Retinopathy

by Huimin Shan, Wenhui Liu, Yangyang Li and Kunpeng Pang

Biomolecules 2023, 13(5), 724; https://doi.org/10.3390/biom13050724 - 23 Apr 2023

Cited by 4 | Viewed by 3770

Abstract

Dry eye disease is a chronic disease of the ocular surface characterized by abnormal tear film composition, tear film instability, and ocular surface inflammation, affecting 5% to 50% of the population worldwide. Autoimmune rheumatic diseases (ARDs) are systemic disorders with multi-organ involvement, including [...] Read more.

Dry eye disease is a chronic disease of the ocular surface characterized by abnormal tear film composition, tear film instability, and ocular surface inflammation, affecting 5% to 50% of the population worldwide. Autoimmune rheumatic diseases (ARDs) are systemic disorders with multi-organ involvement, including the eye, and play a significant role in dry eye. To date, most studies have focused on Sjögren’s syndrome (one of the ARDs) since it manifests as two of the most common symptoms–dry eyes and a dry mouth-and attracts physicians to explore the relationship between dry eye and ARDs. Many patients complained of dry eye related symptoms before they were diagnosed with ARDs, and ocular surface malaise is a sensitive indicator of the severity of ARDs. In addition, ARD related dry eye is also associated with some retinal diseases directly or indirectly, which are described in this review. This review also summarizes the incidence, epidemiological characteristics, pathogenesis, and accompanying ocular lesions of ARD’s related dry eye, emphasizing the potential role of dry eye in recognition and monitoring among ARDs patients. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

13 pages, 1240 KiB

Open AccessFeature PaperEditor’s ChoiceReview

cGMP Signaling in the Neurovascular Unit—Implications for Retinal Ganglion Cell Survival in Glaucoma

by Ameer A. Haider, Tonia S. Rex and Lauren K. Wareham

Biomolecules 2022, 12(11), 1671; https://doi.org/10.3390/biom12111671 - 11 Nov 2022

Cited by 4 | Viewed by 3237

Abstract

Glaucoma is a progressive age-related disease of the visual system and the leading cause of irreversible blindness worldwide. Currently, intraocular pressure (IOP) is the only modifiable risk factor for the disease, but even as IOP is lowered, the pathology of the disease often [...] Read more.

Glaucoma is a progressive age-related disease of the visual system and the leading cause of irreversible blindness worldwide. Currently, intraocular pressure (IOP) is the only modifiable risk factor for the disease, but even as IOP is lowered, the pathology of the disease often progresses. Hence, effective clinical targets for the treatment of glaucoma remain elusive. Glaucoma shares comorbidities with a multitude of vascular diseases, and evidence in humans and animal models demonstrates an association between vascular dysfunction of the retina and glaucoma pathology. Integral to the survival of retinal ganglion cells (RGCs) is functional neurovascular coupling (NVC), providing RGCs with metabolic support in response to neuronal activity. NVC is mediated by cells of the neurovascular unit (NVU), which include vascular cells, glial cells, and neurons. Nitric oxide-cyclic guanosine monophosphate (NO-cGMP) signaling is a prime mediator of NVC between endothelial cells and neurons, but emerging evidence suggests that cGMP signaling is also important in the physiology of other cells of the NVU. NO-cGMP signaling has been implicated in glaucomatous neurodegeneration in humans and mice. In this review, we explore the role of cGMP signaling in the different cell types of the NVU and investigate the potential links between cGMP signaling, breakdown of neurovascular function, and glaucoma pathology. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

27 pages, 1348 KiB

Open AccessReview

Current and Novel Therapeutic Approaches for Treatment of Neovascular Age-Related Macular Degeneration

by Reem H. ElSheikh, Muhammad Z. Chauhan and Ahmed B. Sallam

Biomolecules 2022, 12(11), 1629; https://doi.org/10.3390/biom12111629 - 03 Nov 2022

Cited by 23 | Viewed by 3633

Abstract

Age-related macular degeneration AMD is one of the leading causes of blindness in the elderly population. An advanced form of AMD known as neovascular AMD (nAMD) is implicated as the main attributor of visual loss among these patients. The hallmark feature of nAMD [...] Read more.

Age-related macular degeneration AMD is one of the leading causes of blindness in the elderly population. An advanced form of AMD known as neovascular AMD (nAMD) is implicated as the main attributor of visual loss among these patients. The hallmark feature of nAMD is the presence of neovascular structures known as choroidal neovascular membranes (CNVs), along with fluid exudation, hemorrhages, and subretinal fibrosis. These pathological changes eventually result in anatomical and visual loss. A type of proangiogenic factor known as vascular endothelial growth factor (VEGF) has been known to mediate the pathological process behind nAMD. Therefore, therapy has transitioned over the years from laser therapy that ablates the lesions to using Anti-VEGF to target the pathology directly. In this work, we provide an overview of current and emerging therapies for the treatment of nAMD. Currently approved Anti-VEGF agents include ranibizumab, aflibercept, and brolucizumab. Bevacizumab, also an Anti-VEGF agent, is used to manage nAMD even though this is an off-label use. While Anti-VEGF agents have provided a favorable prognosis for nAMD, they are associated with a substantial financial burden for patients and the healthcare system, due to their high cost as well as the need for frequent repeat treatments and visits. Emerging therapies and studies aim to extend the intervals between required treatments and introduce new treatment modalities that would improve patients’ compliance and provide superior results. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

15 pages, 328 KiB

Open AccessReview

Use of Visual Electrophysiology to Monitor Retinal and Optic Nerve Toxicity

by Tsun-Kang Chiang, Kayla Marie White, Shree K. Kurup and Minzhong Yu

Biomolecules 2022, 12(10), 1390; https://doi.org/10.3390/biom12101390 - 29 Sep 2022

Cited by 4 | Viewed by 2285

Abstract

It is important for clinicians to consider exposure to toxic substances and nutritional deficiencies when diagnosing and managing cases of vision loss. In these cases, physiologic damage can alter the function of key components of the visual pathway before morphologic changes can be [...] Read more.

It is important for clinicians to consider exposure to toxic substances and nutritional deficiencies when diagnosing and managing cases of vision loss. In these cases, physiologic damage can alter the function of key components of the visual pathway before morphologic changes can be detected by traditional imaging methods. Electrophysiologic tests can aid in the early detection of such functional changes to visual pathway components, including the retina or optic nerve. This review provides an overview of various electrophysiologic techniques, including multifocal electroretinogram (mfERG), full-field ERG (ffERG), electrooculogram (EOG), pattern electroretinogram (PERG), and visual evoked potential (VEP) in monitoring the retinal and optic nerve toxicities of alcohol, amiodarone, cefuroxime, cisplatin, deferoxamine, digoxin, ethambutol, hydroxychloroquine, isotretinoin, ocular siderosis, pentosane, PDE5 inhibitors, phenothiazines (chlorpromazine and thioridazine), quinine, tamoxifen, topiramate, vigabatrin, and vitamin A deficiency. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

11 pages, 3505 KiB

Open AccessReview

Clinical and Mechanistic Review of Amiodarone-Associated Optic Neuropathy

by Reece Mitchell and Joseph Chacko

Biomolecules 2022, 12(9), 1298; https://doi.org/10.3390/biom12091298 - 14 Sep 2022

Cited by 3 | Viewed by 1852

Abstract

Amiodarone-associated optic neuropathy (AAON) is a complex clinical diagnosis, requiring distinction from non-arteritic ischemic optic neuropathy (NAION) due to a shared at-risk patient population. Diagnosis of AAON is complicated by a varied clinical presentation and incomplete pathophysiologic mechanisms. This article reviews pertinent literature [...] Read more.

Amiodarone-associated optic neuropathy (AAON) is a complex clinical diagnosis, requiring distinction from non-arteritic ischemic optic neuropathy (NAION) due to a shared at-risk patient population. Diagnosis of AAON is complicated by a varied clinical presentation and incomplete pathophysiologic mechanisms. This article reviews pertinent literature for describing and clinically delineating AAON from NAION, as well as newly reported protective mechanisms of insulin-like growth factor 1 (IGF-1) and PI3K/Akt against amiodarone-induced oxidative and apoptotic injury in retinal ganglion and pigment epithelial cells. These studies offer a basis for exploring mechanisms of amiodarone toxicity in the optic nerve. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

Other

Jump to: Editorial, Research, Review

11 pages, 1112 KiB

Open AccessOpinion

Emerging Role of Adiponectin/AdipoRs Signaling in Choroidal Neovascularization, Age-Related Macular Degeneration, and Diabetic Retinopathy

by Mayank Choubey and Puran Bora

Biomolecules 2023, 13(6), 982; https://doi.org/10.3390/biom13060982 - 13 Jun 2023

Cited by 5 | Viewed by 2077

Abstract

Age-related macular degeneration (AMD), a leading cause of irreversible blindness in adults, may result in poor central vision, making it difficult to see, read, and drive. AMD is generally classified in either dry or wet types. Milder cases of dry AMD may progress [...] Read more.

Age-related macular degeneration (AMD), a leading cause of irreversible blindness in adults, may result in poor central vision, making it difficult to see, read, and drive. AMD is generally classified in either dry or wet types. Milder cases of dry AMD may progress to geographic atrophy (GA), leading to significant visual disability; wet, or neovascular AMD, which involves choroidal neovascularization (CNV), can lead to complete loss of central vision. Adiponectin (APN) discovery in the mid-1990’s and, subsequently, its two cognate receptors (AdipoRs) in the early 2000s have led to a remarkable progress in better understanding metabolic disorders, as well as metabolism-associated ocular pathology. APN/AdipoRs signaling plays a central role in a variety of molecular and cellular physiological events, including glucose and lipid metabolism, whole-body energy regulation, immune and inflammation responses, insulin sensitivity and retinal cell biological functions. This review is an amalgamation of recent information related to APN/AdipoRs in the pathophysiology of retinal diseases and furthers its association with AMD and diabetic retinopathy. Additionally, we present our original research, where we designed control peptide and CNV inhibitory peptide from the globular region of APN to see the effect of these peptides on the mouse model of laser-induced CNV. The inhibitory peptide (APN1) inhibited CNV by more than 75% while the control peptide did not inhibit CNV. Full article

(This article belongs to the Special Issue New Discoveries in Retinal Cell Degeneration and Retinal Diseases)

► Show Figures

Figure 1

Journal Menu

Journal Browser

New Discoveries in Retinal Cell Degeneration and Retinal Diseases

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (14 papers)

Editorial

Research

Review

Other

Further Information

Guidelines

MDPI Initiatives

Follow MDPI