Role of the posterior mucosal defense barrier in portal hypertensive gastropathy - 13/11/21
, Xuemei Liu a, b, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Portal hypertensive gastropathy (PHG) is a complication of cirrhotic or noncirrhotic portal hypertension. PHG is very important in the clinic because it can cause acute or even massive blood loss, and its treatment efficacy and prognosis are poor. Currently, the incidence of PHG in patients with cirrhosis is 20–80%, but its pathogenesis is complicated and poorly understood. Studies have shown that portal hypertension can cause changes in gastric mucosal microcirculation hemodynamics, leading to changes in gastric mucosal histology and function and thereby weakening the mucosal defense barrier. However, no specific drug treatment plans are currently available. This article reviews the current literature to further our understanding of the mechanism underlying PHG and the relationship between PHG and the posterior mucosal defense barrier and to explore new therapeutic targets.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
The pathogenesis of portal hypertensive gastropathy.
Highlights |
• | Endothelial cell injury is the initiating factor in portal hypertensive gastropathy. |
• | Endothelial cell molecules cause dynamic changes in microcirculation perfusion. |
• | There is an interaction between endothelial cell damage and tissue damage. |
• | Anti-oxidation and anti-apoptosis can treat portal hypertensive gastropathy. |
• | Explain the possible molecular mechanism of portal hypertensive gastropathy. |
Abbreviations : AT-II, Akt, Bak, Bax, CAT, ECM, ET-1, EDHF, ERK, eNOS, ER, EGFR, EC, FasL, GPX, GRP78, IL-6, I/R, iNOS, JNK, LPO, MAPK, MKP-1, MOMP, NO, NADPH, NOS, OONO-, PHG, PGI2, PUMA, PCNA, ROS, RNO, SOD, SRC, TEM, TRPV4, TNFR1, TRAIL, TCZ, VEGF, β-Arr1
Keywords : Portal hypertensive gastropathy, Posterior mucosal defense barrier, Microvascular endothelial cells, Ischemia-reperfusion injury, Endothelial cell dysfunction, Endothelial cell molecules
Plan
Vol 144
Article 112258- décembre 2021 Retour au numéro
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