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	<id>https://wikimd.org/index.php?action=history&amp;feed=atom&amp;title=VEGF_receptor</id>
	<title>VEGF receptor - Revision history</title>
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	<updated>2026-04-27T01:44:21Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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		<id>https://wikimd.org/index.php?title=VEGF_receptor&amp;diff=6425556&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
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		<updated>2025-03-04T20:56:19Z</updated>

		<summary type="html">&lt;p&gt;CSV import&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;{{DISPLAYTITLE:VEGF Receptor}}&lt;br /&gt;
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== Introduction ==&lt;br /&gt;
The &amp;#039;&amp;#039;&amp;#039;Vascular Endothelial Growth Factor Receptor&amp;#039;&amp;#039;&amp;#039; (&amp;#039;&amp;#039;&amp;#039;VEGFR&amp;#039;&amp;#039;&amp;#039;) is a type of [[receptor tyrosine kinase]] that plays a crucial role in the regulation of [[angiogenesis]], the process by which new blood vessels form from pre-existing vessels. VEGFRs are primarily expressed on [[endothelial cells]], which line the interior surface of blood vessels, and are activated by binding to [[vascular endothelial growth factor]] (VEGF) ligands.&lt;br /&gt;
&lt;br /&gt;
== Structure ==&lt;br /&gt;
[[File:1djs.jpg|Structure of VEGF receptor|thumb|right]]&lt;br /&gt;
VEGFRs are transmembrane proteins that consist of an extracellular domain, a single transmembrane helix, and an intracellular tyrosine kinase domain. The extracellular domain is responsible for binding to VEGF ligands and is composed of seven immunoglobulin-like domains. The intracellular domain contains the kinase activity necessary for signal transduction.&lt;br /&gt;
&lt;br /&gt;
== Types of VEGF Receptors ==&lt;br /&gt;
There are three main types of VEGF receptors:&lt;br /&gt;
&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;VEGFR-1&amp;#039;&amp;#039;&amp;#039; (Flt-1): This receptor has a high affinity for VEGF-A and is involved in the regulation of [[angiogenesis]] and [[vascular permeability]].&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;VEGFR-2&amp;#039;&amp;#039;&amp;#039; (KDR/Flk-1): This is the principal mediator of the mitogenic, angiogenic, and permeability-enhancing effects of VEGF.&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;VEGFR-3&amp;#039;&amp;#039;&amp;#039; (Flt-4): Primarily involved in [[lymphangiogenesis]], the formation of lymphatic vessels.&lt;br /&gt;
&lt;br /&gt;
== Function ==&lt;br /&gt;
[[File:VEGF_receptors.png|VEGF receptor signaling pathways|thumb|left]]&lt;br /&gt;
Upon binding of VEGF to its receptor, VEGFR undergoes dimerization and autophosphorylation of specific tyrosine residues in the intracellular domain. This activation triggers a cascade of downstream signaling pathways, including the [[PI3K/AKT pathway]], the [[MAPK/ERK pathway]], and the [[PLCγ pathway]], which collectively promote endothelial cell proliferation, migration, and survival.&lt;br /&gt;
&lt;br /&gt;
== Clinical Significance ==&lt;br /&gt;
VEGFRs are critical targets in the treatment of various diseases characterized by abnormal blood vessel growth, such as [[cancer]], [[age-related macular degeneration]], and [[diabetic retinopathy]]. Inhibitors of VEGFR, such as [[sunitinib]] and [[sorafenib]], are used as therapeutic agents to block angiogenesis in tumors, thereby inhibiting tumor growth and metastasis.&lt;br /&gt;
&lt;br /&gt;
== Related Pages ==&lt;br /&gt;
* [[Angiogenesis]]&lt;br /&gt;
* [[Receptor tyrosine kinase]]&lt;br /&gt;
* [[Vascular endothelial growth factor]]&lt;br /&gt;
* [[Endothelial cell]]&lt;br /&gt;
&lt;br /&gt;
[[Category:Receptor tyrosine kinases]]&lt;br /&gt;
[[Category:Cell signaling]]&lt;br /&gt;
[[Category:Angiogenesis]]&lt;/div&gt;</summary>
		<author><name>Prab</name></author>
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