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            Funding text: Angiotensin II-related studies at the Department have been supported by the Hungarian National Science Foundation TO-32019, NK-72661, NK-100883, K-116954, K139231; The Hungarian Society of Hypertension Research Grant 2023 (M.S.); The Hungarian Kidney Foundation; the National Development Agency, Hungary TAMOP 4.2.1.B-09/1/KMR-2010-0001; Hungarian National Research, Development and Innovation NVKP_16-1-2016-0039 and VEKOP-2.3.2-16-2016-00002.</comment>
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      <abstractText>The octapeptide angiotensin II (Ang II) is a circulating hormone as well as a locally formed agonist synthesized by the angiotensin-converting enzyme (ACE) of endothelial cells. It forms a powerful mechanism to control the amount and pressure of body fluids. All main effects are directed to save body salt and water and ensure blood pressure under basic conditions and in emergencies. All blood vessels respond to stimulation by Ang II; the immediate response is smooth muscle contraction, increasing vascular resistance, and elevating blood pressure. Such effects are conveyed by type 1 angiotensin receptors (AT1Rs) located in the plasma membrane of both endothelial and vascular smooth muscle cells. AT1Rs are heterotrimeric G protein-coupled receptors (GPCRs), but their signal pathways are much more complicated than other GPCRs. In addition to Gq/11, the G12/13, JAK/STAT, Jnk, MAPK, and ERK 1/2, and arrestin-dependent and -independent pathways are activated because of the promiscuous attachment of different signal proteins to the intracellular G protein binding site and to the intracellular C terminal loop. Substantial changes in protein expression follow, including the intracellular inflammation signal protein NF-κB, endothelial contact proteins, cytokines, matrix metalloproteinases (MMPs), and type I protocollagen, eliciting the inflammatory transformation of endothelial and vascular smooth muscle cells and fibrosis. Ang II is an important contributor to vascular pathologies in hypertensive, atherosclerotic, and aneurysmal vascular wall remodeling. Such direct vascular effects are reviewed. In addition to reducing blood pressure, AT1R antagonists and ACE inhibitors have a beneficial effect on the vascular wall by inhibiting pathological wall remodeling.</abstractText>
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&lt;div class=&quot;title&quot;&gt;&lt;a href=&quot;/gui2/?mode=browse&amp;params=publication;35651108&quot; target=&quot;_blank&quot;&gt;Direct Vascular Effects of Angiotensin II (A Systematic Short Review)&lt;/a&gt;&lt;/div&gt;    &lt;div&gt;		&lt;span class=&quot;journal-title&quot;&gt;INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES&lt;/span&gt;

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		Paper 113.
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				&lt;div class=&quot;journal-subject&quot;&gt;Folyóirat szakterülete: Scopus - Organic Chemistry&amp;nbsp;&amp;nbsp;&amp;nbsp;SJR indikátor:&amp;nbsp;D1&lt;/div&gt;
				&lt;div class=&quot;journal-subject&quot;&gt;Folyóirat szakterülete: Scopus - Spectroscopy&amp;nbsp;&amp;nbsp;&amp;nbsp;SJR indikátor:&amp;nbsp;D1&lt;/div&gt;
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				&lt;div class=&quot;journal-subject&quot;&gt;Folyóirat szakterülete: Scopus - Molecular Biology&amp;nbsp;&amp;nbsp;&amp;nbsp;SJR indikátor:&amp;nbsp;Q2&lt;/div&gt;
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Forrás	 Idéző
	
	
    | &lt;span class=&quot;type-subtype&quot;&gt;Folyóiratcikk
			( Összefoglaló cikk
			
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      		| &lt;span class=&quot;pub-category&quot;&gt;Tudományos&lt;/span&gt;
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&lt;div class=&quot;funder&quot;&gt; (TO-32019),    (NK-72661),    (NK-100883) Támogató: OTKA,    (K-116954) Támogató: OTKA,    (K139231),    (TÁMOP-4.2.1.B-09/1/KMR-2010–0001) Támogató: TÁMOP,    (NVKP_16-1-2016-0039) Támogató: NKFIH,    (VEKOP-2.3.2-16-2016-00002) Támogató: NKFIH   &lt;/div&gt;
&lt;div class=&quot;lastModified&quot;&gt;Utolsó módosítás: 2026.04.09. 14:45 Sonnevend Kinga (SE_AOK_Élettan_Admin5_SK, admin)
&lt;/div&gt;


        &lt;div class=&quot;lockedBy&quot;&gt;Központi kezelésű 2026.05.28. 12:32  Lévayné Deseő Katalin (MTMT Központi admin)
        &lt;/div&gt;


	&lt;pre class=&quot;comment&quot; style=&quot;margin-top: 0; margin-bottom: 0;&quot;&gt;&lt;u&gt;Megjegyzés&lt;/u&gt;: Funding Agency and Grant Number: Hungarian National Science Foundation [TO-32019, NK-72661, NK-100883, K-116954, K139231]; Hungarian Society of Hypertension Research Grant 2023; Hungarian Kidney Foundation; National Development Agency, Hungary [TAMOP 4.2.1.B-09/1/KMR-2010-0001]; Hungarian National Research, Development and Innovation [NVKP_16-1-2016-0039, VEKOP-2.3.2-16-2016-00002]
            ...&lt;/pre&gt;
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