Inflammation: a way to understanding the evolution of portal hypertension

Aller, María-Ángeles; Arias, Jorge-Luis; Cruz, Arturo; Árias, Jaime

doi:10.1186/1742-4682-4-44

Cited by 63 publications

(101 citation statements)

References 204 publications

(347 reference statements)

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“…Prehepatic portal hypertension by partial portal vein ligation in the rat induces a splanchnic and systemic chronic low-degree inflammatory response that could be developed through the expression of three successive and overlapping phenotypes: ischemia-reperfusion phenotype, immune phenotype and angiogenic phenotype [2,3]. Thus, it has been already proposed that these phenotypes could represent the expression of trophic functional systems with increasing metabolic complexity [2,10].…”

Section: Low-grade Inflammatory Portal Hypertension: the Vitelline Comentioning

confidence: 99%

“…Particularly, in the earliest stage of the embryonic development the vitelline system, as well as the amnion, stands out [7,8] (Figure 1). The portal system, derived from the extraembryonic vitelline venous system continues to perform a vital trophic role for post-natal organism survival and development, although based on its new metabolic needs [2,7]. However, when the portal system suffers an aggression, i.e., portal hypertension, perhaps a regression to the underlying or original embryonic functions could be induced by inflammatory mechanisms [9].…”

Section: Introductionmentioning

confidence: 99%

“…This splanchnic and systemic hemodynamic response would be aggravated during the progression of the chronic liver disease [2,3]. Thus, a critical state is produced in which the appearance of noxious factors during the progressive evolution of chronic liver disease would favor the development of a high-grade splanchnic and systemic inflammatory response [2,4,5].…”

Section: Introductionmentioning

confidence: 99%

“…It could be considered that the underlying central theme in low-grade portal hypertensive inflammation is the disturbance in splanchnic and systemic hemodynamics [1,2]. This splanchnic and systemic hemodynamic response would be aggravated during the progression of the chronic liver disease [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…It has been proposed that low-grade inflammation related to portal hypertension switches to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease [2].…”

Section: Introductionmentioning

confidence: 99%

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Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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Section: Low-grade Inflammatory Portal Hypertension: the Vitelline Comentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

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Aquaporin-1 is associated with arterial capillary proliferation and hepatic sinusoidal transformation contributing to portal hypertension in primary biliary cirrhosis

et al. 2013

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Although aquaporins (AQPs) in normal hepatobiliary system have been studied, little is known about AQP localization and changes in the hepatic microvascular system including sinusoids in cholestatic liver. The present study aimed to clarify the localization of AQP-1 in the microvessels in normal human liver and in primary biliary cirrhosis (PBC). Human normal liver (control) and PBC liver specimens were obtained. Immunohistochemistry, Western blotting, in situ hybridization (ISH) and electron microscopic examination for AQP-1 were conducted. In control liver and stages I-II PBC liver, AQP-1 immunoreactivity was mainly localized in portal venules, hepatic arterioles and bile ducts in the portal tract, but was hardly detected in the sinusoids. However, AQP-1 expression was enhanced in the proliferated bile ductules in PBC. In stages III-IV PBC liver tissues, AQP-1 was aberrantly expressed in proliferated arterial capillaries opening into the sinusoids at the peripheral edge of regenerating hepatic nodules and in the fibrotic septa. Overexpression of AQP-1 at protein and mRNA levels was demonstrated by Western blot and ISH, respectively. Angiogenetic and fibrotic responses are probably induced by AQP-1, leading to enhanced pouring of arterial blood into the sinusoids; thus, contributing to progression of portal hypertension in PBC.

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Gut-Brain Chemokine Changes in Portal Hypertensive Rats

et al. 2011

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Inflammation: a way to understanding the evolution of portal hypertension

Abstract: Background: Portal hypertension is a clinical syndrome that manifests as ascites, portosystemic encephalopathy and variceal hemorrhage, and these alterations often lead to death.

Cited by 63 publications

References 204 publications

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aquaporin-1 is associated with arterial capillary proliferation and hepatic sinusoidal transformation contributing to portal hypertension in primary biliary cirrhosis

Gut-Brain Chemokine Changes in Portal Hypertensive Rats

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