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Do anti-VEGFs used in the ophthalmic clinic cause Müller glial cell stress?
Rafael André da Silvaa,
Corresponding author
rafaels@usp.br

Corresponding author.
, Luiz Philipe de Souza Ferreirab, Vinicius Moraes de Paiva Rodac, José Maria Soares Juniord, Manuel de Jesus Simõesb, Caio Vinicius Saito Regatierie
a Biosciences Graduate Program, Institute of Biosciences, Instituto de Biociências, Letras e Ciências Exatas, Universidade Estadual Paulista (IBILCE/UNESP), São José do Rio Preto, SP, Brazil
b Structural and Functional Biology Graduate Program, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil
c Life Systems Biology Graduate Program, Instituto de Ciências Biomédicas, Universidade de São Paulo (ICB/USP), São Paulo, SP, Brazil
d Department of Obstetrics and Gynecology, Faculdade de Medicina, Universidade de São Paulo (FMUSP), São Paulo, SP, Brazil
e Department of Ophthalmology, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="para0001" class="elsevierStylePara elsevierViewall">Age-related Macular Degeneration &#40;AMD&#41; and Diabetic Retinopathy &#40;DR&#41; are eye diseases that can lead to vision loss&#46; AMD mainly affects the elderly and DR individuals of different ages&#46;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a> M&#252;ller Glial Cells &#40;MGCs&#41; play a crucial role in the pathogenesis of these diseases&#44; modulating inflammation and angiogenesis&#46;<a class="elsevierStyleCrossRef" href="#bib0003"><span class="elsevierStyleSup">3</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0004"><span class="elsevierStyleSup">4</span></a> Activated MGCs in gliosis overexpress Glial Fibrillary Acid Protein &#40;GFAP&#41; and actively produce Vascular Endothelial Growth Factor &#40;VEGF&#41;&#44; leading to abnormal retinal angiogenesis and microinflammation&#46;<a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">5</span></a> To manipulate the main signaling pathway involved in neovascular AMD and DR&#44; anti-VEGF drugs are used intravitreally in the ophthalmic clinic&#44; including ranibizumab&#44; bevacizumab&#44; aflibercept and brolucizumab&#46;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a> However&#44; little is known about the impact of anti-VEGF medications on M&#252;ller cells&#46;</p><p id="para0002" class="elsevierStylePara elsevierViewall">In vitro&#44; primary MGC cells&#44; retinal cells in organotypic culture&#44; as well as human M&#252;ller cells line &#40;MIO-M1&#41; treated with aflibercept&#44; ranibizumab&#44; or bevacizumab show time-dependent increased GFAP expression&#46;<a class="elsevierStyleCrossRefs" href="#bib0006"><span class="elsevierStyleSup">6&#8211;9</span></a> Aflibercept and Ranibizumab regulate GFAP positively via pERK1&#47;2&#46;<a class="elsevierStyleCrossRef" href="#bib0006"><span class="elsevierStyleSup">6</span></a> In rabbits&#44; ziv-aflibercept&#44; although it does not change the electroretinogram&#44; increases the expression of GFAP&#44; suggesting retinal stress caused by the drug&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">10</span></a></p><p id="para0003" class="elsevierStylePara elsevierViewall">MIO-M1 cells&#44; treated during 24&#160;h with anti-VEGF drugs&#44; show a reduction of these cells&#8217; metabolism&#46; Additionally&#44; there is an increase of reactive oxygen species and expression of the pro-inflammatory interleukin IL-&#946; which are apoptosis markers&#46;<a class="elsevierStyleCrossRef" href="#bib0011"><span class="elsevierStyleSup">11</span></a> Bevacizumab positively regulates the apoptosis of M&#252;ller cells via caspase-3&#46;<a class="elsevierStyleCrossRef" href="#bib0007"><span class="elsevierStyleSup">7</span></a> Conversely in another study&#44; aflibercept and ranibizumab in 24&#160;h do not affect cell survival&#46; Furthermore&#44; mitochondrial and cytoplasmic stress were observed through HSP60 and HSP90 in MIO-M1 cells&#46;<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a></p><p id="para0004" class="elsevierStylePara elsevierViewall">Anti-VEGF drugs are efficient to treat AMD and DR&#44;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0013"><span class="elsevierStyleSup">13</span></a> therefore&#44; so far&#44; through the data available in the literature&#44; we must consider that M&#252;ller cells can undergo cellular stress&#44; evidenced by the main gliosis marker&#44; GFAP&#46; In addition&#44; anti-VEGF drugs can disrupt the metabolism of these cells&#46; It is important at this time that we carry out translational studies in humans to investigate the points highlighted here&#46; Cohort studies&#44; considering the long treatment inpatients&#44; show retinal atrophy and fibrosis&#44;<a class="elsevierStyleCrossRef" href="#bib0014"><span class="elsevierStyleSup">14</span></a> which may be related to gliosis and resistance to anti-VEGFs in some patients with AMD and RD&#46;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a></p><p id="para0005" class="elsevierStylePara elsevierViewall">We can find different results of MGCs&#8217; gliosis and survival under the influence of anti-VEGF drugs&#59; this may be related to the particular molecular mechanism of each drug&#46; Among the anti-VEGF drugs used in the ophthalmic clinic for AMD and PDR&#44; brolucizumab was not investigated in MGCs&#46; Although we have evidence that anti-VEGF drugs can lead to gliosis of MGCs&#44; more studies are needed to understand the mechanisms around this stress&#46; It is essential to understand these mechanisms for a possible improvement of existing drugs and facilitate new therapeutic interventions with fewer side effects&#46;</p></span>"
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ISSN: 18075932
Original language: English
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