Portal hypertensive cardiovascular pathology: The rescue of ancestral survival mechanisms?

Aller, María-Ángeles; Heras, Natalia de las; Blanco-Rivero, Javier; Arias, Jorge-Luis; Lahera, Vicente; Balfagón, Gloria; Árias, Jaime

doi:10.1016/j.clinre.2011.07.017

Cited by 9 publications

(11 citation statements)

References 107 publications

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“…After operation, the process of wound healing starts immediately with mainly three overlapping phases of inflammation, proliferation and remodeling, of which the inflammation phase essentially leads to the next phase [42]. Any factors interfering with the normal inflammatory phase will influence the transition from the inflammatory to the proliferative phase which represents a key step during wound healing [43].…”

Section: Discussionmentioning

confidence: 99%

Reduction of Inflammatory Response by Way of Oxidative Stress with San Huang Decoction (SHD) In Perioperative Care: A Randomized Clinical Trial

Yu¹,

Weihe²,

Xu³

et al. 2017

IJCAM

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Section: Discussionmentioning

confidence: 99%

Reduction of Inflammatory Response by Way of Oxidative Stress with San Huang Decoction (SHD) In Perioperative Care: A Randomized Clinical Trial

Yu¹,

Weihe²,

Xu³

et al. 2017

IJCAM

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“…intrahepatic. The partial portal vein ligation, or compensated, and the extrahepatic cholestasis or decompensated, are the experimental models most frequently used to study both types of portal hypertension [190]. Prehepatic portal hypertension by partial portal vein ligation in the rat induces the expression of three overlapping phenotypes, whose pathophysiological mechanisms recall those that are associated with the yolk sac development or vitallogenics.…”

Section: Discussionmentioning

confidence: 99%

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

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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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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“…In this line, recent evidence supports a relationship between NAFLD and cardiovascular disease[50,55]. Particularly in TPVL-rats NASH, this association could be considered a risk factor for a wound-like inflammatory aortic response[49], with increased expression of NF-κB, TNF-α, IL-1β and IL-6 in the aortic wall[48,49]. …”

Section: The Immune Inflammatory Phenotypementioning

confidence: 97%

“…The immune phenotype could be coupled with bacterial intestinal translocation to mesenteric lymph nodes, increased mast cells in the splanchnic area, an acute phase response, dyslipidemia and hepatic steatosis[43]. We have shown that splanchnic and systemic inflammatory changes develop in TPVL-rats, including portal hypertensive enteropathy[43,44], mesenteric adenitis[45,46], portal hypertensive encephalopathy[47], liver steatosis[8-10], aortic atherosclerosis-like disease[48-50] and metabolic syndrome[51]. …”

Section: The Immune Inflammatory Phenotypementioning

confidence: 99%

Embrionary way to create a fatty liver in portal hypertension

Aller

Arias

Peral

et al. 2017

WJGP

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Portal hypertension in the rat by triple partial portal vein ligation produces an array of splanchnic and systemic disorders, including hepatic steatosis. In the current review these alterations are considered components of a systemic inflammatory response that would develop through three overlapping phenotypes: The neurogenic, the immune and the endocrine. These three inflammatory phenotypes could resemble the functions expressed during embryonic development of mammals. In turn, the inflammatory phenotypes would be represented in the embryo by two functional axes, that is, a coelomic-amniotic axis and a trophoblastic yolk-sac or vitelline axis. In this sense, the inflammatory response developed after triple partial portal vein ligation in the rat would integrate both functional embryonic axes on the liver interstitial space of Disse. If so, this fact would favor the successive development of steatosis, steatohepatitis and fibrosis. Firstly, these recapitulated embryonic functions would produce the evolution of liver steatosis. In this way, this fat liver could represent a yolk-sac-like in portal hypertensive rats. After that, the systemic recapitulation of these embryonic functions in experimental prehepatic portal hypertension would consequently induce a gastrulation-like response in which a hepatic wound healing reaction or fibrosis occur. In conclusion, studying the mechanisms involved in embryonic development could provide key results for a better understanding of the nonalcoholic fatty liver disease etiopathogeny.

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Portal hypertensive cardiovascular pathology: The rescue of ancestral survival mechanisms?

Cited by 9 publications

References 107 publications

Reduction of Inflammatory Response by Way of Oxidative Stress with San Huang Decoction (SHD) In Perioperative Care: A Randomized Clinical Trial

Reduction of Inflammatory Response by Way of Oxidative Stress with San Huang Decoction (SHD) In Perioperative Care: A Randomized Clinical Trial

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

Embrionary way to create a fatty liver in portal hypertension

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