Innate Immune Response in Hypertension

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F22%3A73617624" target="_blank" >RIV/61989592:15110/22:73617624 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.eurekaselect.com/article/126523" target="_blank" >https://www.eurekaselect.com/article/126523</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.2174/1381612828666220922112412" target="_blank" >10.2174/1381612828666220922112412</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Innate Immune Response in Hypertension

Popis výsledku v původním jazyce

Even though an association between inflammation and hypertension has been known for many years, it has not been simple to ascertain the role of several physiological responses involved. The innate immune response plays a critical role in these physiological responses. Innate immune cells can be activated directly by shear stress, activate the inflammasome and produce numerous cytokines and soluble mediators essential in hypertension. NFkB activation is mainly involved in the activation of innate immune cells. Shear stress also stimulates the expression of DAMP and PAMP receptors, enhancing pathogen and danger signals and magnifying inflammation. The adaptative immune response is activated with the increased antigen presentation resulting from the insults mentioned. Chronic inflammation may lead to autoimmunity. Peripheral hypoxia, a consequence of hypertension, activates hypoxia-inducing factors 1-alpha and 1-beta (HIF-1 alpha, HIF-1 beta), which modulate innate immune cells and promote inflammation. HIF-1 alpha is involved in the upregulation of oxygen and nitrogen radical production proteins. HIF-1 beta down-regulates antioxidant enzymes. However, the critical evidence of the role of innate immune cells in hypertension came from the results of clinical trials involving therapies blocking inflammatory cytokines and Toll-like receptor expression. Several lines of research have been conducted on this complex disease. Pro-tolerogenic innate immune cells, myeloid suppressor cells, and M2 macrophages may play a crucial role in promoting or resolving inflammation, cardiovascular diseases and hypertension, and should be studied in detail.

Název v anglickém jazyce

Innate Immune Response in Hypertension

Popis výsledku anglicky

Even though an association between inflammation and hypertension has been known for many years, it has not been simple to ascertain the role of several physiological responses involved. The innate immune response plays a critical role in these physiological responses. Innate immune cells can be activated directly by shear stress, activate the inflammasome and produce numerous cytokines and soluble mediators essential in hypertension. NFkB activation is mainly involved in the activation of innate immune cells. Shear stress also stimulates the expression of DAMP and PAMP receptors, enhancing pathogen and danger signals and magnifying inflammation. The adaptative immune response is activated with the increased antigen presentation resulting from the insults mentioned. Chronic inflammation may lead to autoimmunity. Peripheral hypoxia, a consequence of hypertension, activates hypoxia-inducing factors 1-alpha and 1-beta (HIF-1 alpha, HIF-1 beta), which modulate innate immune cells and promote inflammation. HIF-1 alpha is involved in the upregulation of oxygen and nitrogen radical production proteins. HIF-1 beta down-regulates antioxidant enzymes. However, the critical evidence of the role of innate immune cells in hypertension came from the results of clinical trials involving therapies blocking inflammatory cytokines and Toll-like receptor expression. Several lines of research have been conducted on this complex disease. Pro-tolerogenic innate immune cells, myeloid suppressor cells, and M2 macrophages may play a crucial role in promoting or resolving inflammation, cardiovascular diseases and hypertension, and should be studied in detail.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30104 - Pharmacology and pharmacy

Projekt

<a href="/cs/project/EF16_019%2F0000868" target="_blank" >EF16_019/0000868: Molekulární, buněčný a klinický přístup ke zdravému stárnutí</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2022

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

CURRENT PHARMACEUTICAL DESIGN

ISSN

1381-6128

e-ISSN

1873-4286

Svazek periodika

28

Číslo periodika v rámci svazku

36

Stát vydavatele periodika

AE - Spojené arabské emiráty

Počet stran výsledku

7

Strana od-do

2984-2990

Kód UT WoS článku

000892876800005

EID výsledku v databázi Scopus

2-s2.0-85141400377