Progress in Retinal and Eye Research最新文献

{"title":"The pre-Descemet's layer (Dua's layer, also known as the Dua-Fine layer and the pre-posterior limiting lamina layer): Discovery, characterisation, clinical and surgical applications, and the controversy","authors":"Harminder S. Dua ,&nbsp;Rui Freitas ,&nbsp;Imran Mohammed ,&nbsp;Darren S.J. Ting ,&nbsp;Dalia G. Said","doi":"10.1016/j.preteyeres.2022.101161","DOIUrl":"10.1016/j.preteyeres.2022.101161","url":null,"abstract":"<div><p>The pre-Descemet's layer/Dua's layer, also termed the Dua-Fine layer and the pre-posterior limiting lamina layer, lies anterior to the Descemet's membrane in the cornea, is 10 μm (range 6–16) thick, made predominantly of type I and some type VI collagen with abundant elastin, more than any other layer of the cornea. It has high tensile strength (bursting pressure up to 700 mm of Hg), is impervious to air and almost acellular. At the periphery it demonstrates fenestrations and ramifies to become the core of the trabecular meshwork, with implications for intraocular pressure and glaucoma. It has been demonstrated in some species of animals.</p><p>The layer has assumed considerable importance in anterior and posterior lamellar corneal transplant surgery by improving our understanding of the behaviour of corneal tissue during these procedures, improved techniques and made the surgery safer with better outcomes. It has led to the innovation of new surgical procedures namely, pre-Descemet's endothelial keratoplasty, suture management of acute hydrops, DALK-triple and Fogla's mini DALK.</p><p>The discovery and knowledge of the layer has introduced paradigm shifts in our age old concepts of Descemet's membrane detachment, acute corneal hydrops in keratoconus and Descemetoceles, with impact on management approaches. It has been shown to contribute to the pathology and clinical signs observed in corneal infections and some corneal dystrophies. Early evidence suggests that it may have a role in the pathogenesis of keratoconus in relation to its elastin content. Its contribution to corneal biomechanics and glaucoma are subjects of current investigations.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101161"},"PeriodicalIF":17.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1350946222001215/pdfft?md5=a70dbcd5811aec9179e2fef22e02ebb3&pid=1-s2.0-S1350946222001215-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9080188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genetics and disease mechanisms of rhegmatogenous retinal detachment","authors":"Birgit M. Govers ,&nbsp;Ramon A.C. van Huet ,&nbsp;Susanne Roosing ,&nbsp;Sander Keijser ,&nbsp;Leonoor I. Los ,&nbsp;Anneke I. den Hollander ,&nbsp;B. Jeroen Klevering","doi":"10.1016/j.preteyeres.2022.101158","DOIUrl":"10.1016/j.preteyeres.2022.101158","url":null,"abstract":"<div><p>Rhegmatogenous retinal detachment (RRD) is a sight threatening condition that warrants immediate surgical intervention. To date, 29 genes have been associated with monogenic disorders involving RRD. In addition, RRD can occur as a multifactorial disease through a combined effect of multiple genetic variants and non-genetic risk factors. In this review, we provide a comprehensive overview of the spectrum of hereditary disorders involving RRD. We discuss genotype-phenotype correlations of these monogenic disorders, and describe genetic variants associated with RRD through multifactorial inheritance. Furthermore, we evaluate our current understanding of the molecular disease mechanisms of RRD-associated genetic variants on collagen proteins, proteoglycan versican, and the TGF-β pathway. Finally, we review the role of genetics in patient management and prevention of RRD. We provide recommendations for genetic testing and prophylaxis of at-risk patients, and hypothesize on novel therapeutic approaches beyond surgical intervention.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101158"},"PeriodicalIF":17.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1350946222001185/pdfft?md5=3c19118a48af3c4fda7c893f2d972f86&pid=1-s2.0-S1350946222001185-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10847257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the contribution of ARMS2 and HTRA1 genetic risk factors in age-related macular degeneration","authors":"Yang Pan ,&nbsp;Yingbin Fu ,&nbsp;Paul N. Baird ,&nbsp;Robyn H. Guymer ,&nbsp;Taraprasad Das ,&nbsp;Takeshi Iwata","doi":"10.1016/j.preteyeres.2022.101159","DOIUrl":"10.1016/j.preteyeres.2022.101159","url":null,"abstract":"<div><p><span><span>Age-related macular degeneration (AMD) is the leading cause of severe irreversible central vision loss in individuals over 65 years old. Genome-wide association studies (GWASs) have shown that the region at chromosome 10q26, where the age-related </span>maculopathy susceptibility (</span><em>ARMS2/LOC387715</em><span>) and HtrA serine peptidase 1 (</span><em>HTRA1</em>) genes are located, represents one of the strongest associated loci for AMD. However, the underlying biological mechanism of this genetic association has remained elusive. In this article, we extensively review the literature by us and others regarding the <em>ARMS2/HTRA1</em><span><span><span> risk alleles and their functional significance. We also review the literature regarding the presumed function of the ARMS2 protein and the molecular processes<span> of the HTRA1 protein in AMD pathogenesis in vitro and in vivo, including those of transgenic mice overexpressing HtrA1/HTRA1 which developed </span></span>Bruch's membrane (BM) damage, </span>choroidal neovascularization<span> (CNV), and polypoidal choroidal vasculopathy (PCV), similar to human AMD patients. The elucidation of the molecular mechanisms of the </span></span><em>ARMS2</em> and <em>HTRA1</em><span><span> susceptibility loci has begun to untangle the complex biological pathways underlying AMD pathophysiology, pointing to new testable paradigms for </span>treatment.</span></p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101159"},"PeriodicalIF":17.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10454125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Consensus and controversies in the science of endophthalmitis management: Basic research and clinical perspectives","authors":"Taraprasad Das ,&nbsp;Joveeta Joseph ,&nbsp;Matthew P. Simunovic ,&nbsp;Andrzej Grzybowski ,&nbsp;Kuan-Jen Chen ,&nbsp;Vivek Pravin Dave ,&nbsp;Savitri Sharma ,&nbsp;Patrick Staropoli ,&nbsp;Harry Flynn Jr.","doi":"10.1016/j.preteyeres.2023.101218","DOIUrl":"10.1016/j.preteyeres.2023.101218","url":null,"abstract":"<div><p>Infectious endophthalmitis<span><span> is a severe intraocular infection caused by bacteria, or less commonly by fungi. It can occur after penetrating eye procedures, trauma, or the spread of infection from contiguous structures or via emboli from distant organs. Because of the time-critical nature of the treatment, </span>endophthalmitis<span> is treated with the clinical diagnosis and modified by the microbiological report of the intraocular contents. The current strategy for managing endophthalmitis relies on pre-clinical literature, case series, and one large multi-center randomized clinical trial on post-cataract surgery endophthalmitis. Culture-susceptibility of the microorganisms from undiluted vitreous guides the definitive treatment in non-responsive cases. Strategies to reduce the incidence of endophthalmitis after penetrating eye procedures have been developed concurrently with refined means of treatment.</span></span></p><p>Despite these advances, outcomes remain poor for many patients. Although consensus articles have been published on managing endophthalmitis, treatment patterns vary, and controversies remain. These include (1) the use of newer methods for early and precise microbiological diagnosis; (2) the choice of intravitreal antibiotics; (3) the need for systemic therapy; (4) early and complete vitrectomy. Here, we review the current consensus and address controversies in diagnosing and managing endophthalmitis. This review is intended to familiarize physicians and ophthalmologists with different aspects of endophthalmitis management to make informed decisions.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101218"},"PeriodicalIF":17.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41211034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurovascular dysfunction in glaucoma","authors":"Luis Alarcon-Martinez ,&nbsp;Yukihiro Shiga ,&nbsp;Deborah Villafranca-Baughman ,&nbsp;Jorge L. Cueva Vargas ,&nbsp;Isaac A. Vidal Paredes ,&nbsp;Heberto Quintero ,&nbsp;Brad Fortune ,&nbsp;Helen Danesh-Meyer ,&nbsp;Adriana Di Polo","doi":"10.1016/j.preteyeres.2023.101217","DOIUrl":"10.1016/j.preteyeres.2023.101217","url":null,"abstract":"<div><p>Retinal ganglion cells, the neurons that die in glaucoma, are endowed with a high metabolism requiring optimal provision of oxygen and nutrients to sustain their activity. The timely regulation of blood flow is, therefore, essential to supply firing neurons in active areas with the oxygen and glucose they need for energy. Many glaucoma patients suffer from vascular deficits including reduced blood flow, impaired autoregulation, neurovascular coupling dysfunction, and blood-retina/brain-barrier breakdown. These processes are tightly regulated by a community of cells known as the neurovascular unit comprising neurons, endothelial cells, pericytes, Müller cells, astrocytes, and microglia. In this review, the neurovascular unit takes center stage as we examine the ability of its members to regulate neurovascular interactions and how their function might be altered during glaucomatous stress. Pericytes receive special attention based on recent data demonstrating their key role in the regulation of neurovascular coupling in physiological and pathological conditions. Of particular interest is the discovery and characterization of tunneling nanotubes, thin actin-based conduits that connect distal pericytes, which play essential roles in the complex spatial and temporal distribution of blood within the retinal capillary network. We discuss cellular and molecular mechanisms of neurovascular interactions and their pathophysiological implications, while highlighting opportunities to develop strategies for vascular protection and regeneration to improve functional outcomes in glaucoma.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101217"},"PeriodicalIF":17.8,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41146037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors, clinical features and treatment of Behçet's disease uveitis","authors":"Zhenyu Zhong,&nbsp;Guannan Su,&nbsp;Peizeng Yang","doi":"10.1016/j.preteyeres.2023.101216","DOIUrl":"10.1016/j.preteyeres.2023.101216","url":null,"abstract":"<div><p><span><span><span>Behçet's disease is a </span>systemic vasculitis<span><span><span> frequently associated with intraocular inflammation. Recent findings identified independent clinical clusters in Behçet's disease, each involving distinct combinations of affected organs. Ocular Behçet's disease, mainly manifested as uveitis, is characterized as an independent cluster with a low likelihood of association with other system involvements, such as intestinal, cardiovascular, or </span>central nervous system. A prevailing theory suggests that the pathogenesis of the disease is multifactorial, where a variety of genetic and infectious agents may interact with each other to cause the disease. Among sporadic cases, the </span>human leukocyte antigen (HLA) genes, including HLA-B51, HLA-A26, HLA-B15, and HLA-B5701, have been found to be a key component conferring </span></span>genetic susceptibility<span>. Outside the HLA region, a set of susceptibility variants are identified, closely related to interleukin (IL)-23/IL-17 pathway, tumor necrosis factor<span> (TNF) signaling, and pattern recognition receptor systems. Microbial infections, such as </span></span></span><span><em>Streptococcus sanguinis</em></span>, <span><em>Mycobacterium tuberculosis</em></span><span><span><span><span>, and Herpes simplex virus (HSV), are linked to play the triggering of disease in immunogenetically predisposed individuals. Clinically, due to the notable relapsing-remitting course of ocular Behçet's disease, the prevention of recurrent attack would be the primary </span>treatment goal. Combination of corticosteroids and </span>immunomodulatory drugs, such as anti-TNF agents, </span>interferon<span><span>, and conventional immunosuppressants (e.g. </span>cyclosporine<span>, azathioprine), have been the mainstream regimen for the disease. Future research may focus on comparing the effectiveness of immunomodulatory drugs and identifying the most suitable subgroups for a specific drug on the basis of the knowledge of the molecular heterogeneity of the disease.</span></span></span></p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"97 ","pages":"Article 101216"},"PeriodicalIF":17.8,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41169708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neville Osborne - Editor-in-Chief of Progress in Retinal and Eye Research for 40 years","authors":"Leopold Schmetterer,&nbsp;Gülgün Tezel,&nbsp;Joel Schuman","doi":"10.1016/j.preteyeres.2023.101194","DOIUrl":"10.1016/j.preteyeres.2023.101194","url":null,"abstract":"","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"96 ","pages":"Article 101194"},"PeriodicalIF":17.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10301420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"10q26 – The enigma in age-related macular degeneration","authors":"David A. Merle ,&nbsp;Merve Sen ,&nbsp;Angela Armento ,&nbsp;Chloe M. Stanton ,&nbsp;Eric F. Thee ,&nbsp;Magda A. Meester-Smoor ,&nbsp;Markus Kaiser ,&nbsp;Simon J. Clark ,&nbsp;Caroline C.W. Klaver ,&nbsp;Pearse A. Keane ,&nbsp;Alan F. Wright ,&nbsp;Michael Ehrmann ,&nbsp;Marius Ueffing","doi":"10.1016/j.preteyeres.2022.101154","DOIUrl":"10.1016/j.preteyeres.2022.101154","url":null,"abstract":"<div><p>Despite comprehensive research efforts over the last decades, the pathomechanisms of age-related macular degeneration (AMD) remain far from being understood. Large-scale genome wide association studies (GWAS) were able to provide a defined set of genetic aberrations which contribute to disease risk, with the strongest contributors mapping to distinct regions on chromosome 1 and 10. While the chromosome 1 locus comprises factors of the complement system with well-known functions, the role of the 10q26-locus in AMD-pathophysiology remains enigmatic. 10q26 harbors a cluster of three functional genes, namely <em>PLEKHA1</em>, <em>ARMS2</em> and <em>HTRA1</em>, with most of the AMD-associated genetic variants mapping to the latter two genes. High linkage disequilibrium between <em>ARMS2</em> and <em>HTRA1</em> has kept association studies from reliably defining the risk-causing gene for long and only very recently the genetic risk region has been narrowed to <em>ARMS2</em>, suggesting that this is the true AMD gene at this locus. However, genetic associations alone do not suffice to prove causality and one or more of the 14 SNPs on this haplotype may be involved in long-range control of gene expression, leaving <em>HTRA1</em> and <em>PLEKHA1</em> still suspects in the pathogenic pathway. Both, <em>ARMS2</em> and <em>HTRA1</em> have been linked to extracellular matrix homeostasis, yet their exact molecular function as well as their role in AMD pathogenesis remains to be uncovered. The transcriptional regulation of the 10q26 locus adds an additional level of complexity, given, that gene-regulatory as well as epigenetic alterations may influence expression levels from 10q26 in diseased individuals. Here, we provide a comprehensive overview on the 10q26 locus and its three gene products on various levels of biological complexity and discuss current and future research strategies to shed light on one of the remaining enigmatic spots in the AMD landscape.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"96 ","pages":"Article 101154"},"PeriodicalIF":17.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10280074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The novel role of lymphatic vessels in the pathogenesis of ocular diseases","authors":"Thomas Clahsen ,&nbsp;Karina Hadrian ,&nbsp;Maria Notara ,&nbsp;Simona L. Schlereth ,&nbsp;Antonia Howaldt ,&nbsp;Verena Prokosch ,&nbsp;Thomas Volatier ,&nbsp;Deniz Hos ,&nbsp;Falk Schroedl ,&nbsp;Alexandra Kaser-Eichberger ,&nbsp;Ludwig M. Heindl ,&nbsp;Philipp Steven ,&nbsp;Jacobus J. Bosch ,&nbsp;Alexander Steinkasserer ,&nbsp;Alexander C. Rokohl ,&nbsp;Hanhan Liu ,&nbsp;Mert Mestanoglu ,&nbsp;Hamid Kashkar ,&nbsp;Björn Schumacher ,&nbsp;Friedemann Kiefer ,&nbsp;Claus Cursiefen","doi":"10.1016/j.preteyeres.2022.101157","DOIUrl":"10.1016/j.preteyeres.2022.101157","url":null,"abstract":"<div><p><span>Historically, the eye has been considered as an organ free of lymphatic vessels. In recent years, however, it became evident, that lymphatic vessels or lymphatic-like vessels contribute to several </span>ocular pathologies at various peri- and intraocular locations. The aim of this review is to outline the pathogenetic role of ocular lymphatics, the respective molecular mechanisms and to discuss current and future therapeutic options based thereon.</p><p><span><span><span><span><span>We will give an overview on the vascular anatomy<span> of the healthy ocular surface<span><span> and the molecular mechanisms contributing to corneal (lymph)angiogenic privilege. In addition, we present (i) current insights into the cellular and molecular mechanisms occurring during pathological neovascularization of the cornea triggered e.g. by inflammation or trauma, (ii) the role of lymphatic vessels in different ocular surface pathologies such as dry eye disease, </span>corneal graft rejection, ocular </span></span></span>graft versus host disease, allergy, and </span>pterygium, (iii) the involvement of lymphatic vessels in </span>ocular tumors<span> and metastasis, and (iv) the novel role of the lymphatic-like structure of </span></span>Schlemm's canal<span><span> in glaucoma. Identification of the underlying molecular mechanisms and of novel modulators of lymphangiogenesis<span> will contribute to the development of new therapeutic targets for the treatment of ocular diseases associated with pathological lymphangiogenesis in the future. The preclinical data presented here outline novel therapeutic concepts for promoting </span></span>transplant survival, inhibiting metastasis of ocular tumors, reducing inflammation of the ocular surface, and treating glaucoma. Initial data from </span></span>clinical trials suggest first success of novel treatment strategies to promote transplant survival based on pretransplant corneal lymphangioregression.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"96 ","pages":"Article 101157"},"PeriodicalIF":17.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10330029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etiopathogenesis of primary acquired nasolacrimal duct obstruction (PANDO)","authors":"Mohammad Javed Ali","doi":"10.1016/j.preteyeres.2023.101193","DOIUrl":"10.1016/j.preteyeres.2023.101193","url":null,"abstract":"<div><p>Primary acquired nasolacrimal duct obstruction, or PANDO, is a common adult lacrimal drainage disorder. The current treatment modality of dacryocystorhinostomy to bypass the obstructed nasolacrimal duct has excellent outcomes. However, the understanding of the disease etiopathogenesis needs to be revisited. There are not many studies that specifically assessed any hypothesis or ones that convincingly put forth the presumed or confirmed interpretations regarding the PANDO pathogenesis or the mechanisms or pathways involved therein. Histopathological evidence points to recurrent inflammation of the nasolacrimal duct, subsequent fibrosis, and the resultant obstruction. The disease etiopathogenesis is considered multifactorial. Several implicated suspects include anatomical narrowing of the bony nasolacrimal duct, vascular factors, local hormonal imbalance, microbial influence, nasal abnormalities, autonomic dysregulation, surfactants, lysosomal dysfunction, gastroesophageal reflux, tear proteins, and deranged local host defenses. The present work reviewed the literature on the etiopathogenesis of primary acquired nasolacrimal duct obstruction (PANDO) to gain insights into the present state of the understanding and the high-value translational implications of precisely decoding the disease etiology.</p></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"96 ","pages":"Article 101193"},"PeriodicalIF":17.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10282580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}