Pitavastatin Enhances the Anti-Fibrogenesis Effects of Candesartan, an Angiotensin Ⅱ Receptor Blocker, on CCl&lt;sub&gt;4&lt;/sub&gt;-Induced Liver Fibrosis in Rats

Nie, Lianbo; Imamura, Michio; Itoh, Hideaki; Ueno, Hikaru

doi:10.7888/juoeh.26.165

Cited by 16 publications

(15 citation statements)

References 4 publications

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“…Taken together, these findings suggest that atorvastatin abrogates the activation of quiescent HSC in beginning fibrosis. Although no significant prophylactic effect of statins on fibrosis was shown in previous investigations [20,21], these studies suggested an effect on collagen synthesis [9] as well as on angiotensin II-induced inflammation and fibrosis [19,20]. The lack of clear prophylactic antifibrotic effects might be explained by very low doses of statins in these investigations [19][20][21].…”

Section: Discussionmentioning

confidence: 64%

“…The lack of clear prophylactic antifibrotic effects might be explained by very low doses of statins in these investigations [19][20][21]. Nevertheless, these groups also found benefits of statins, when combined with angiotensin II type 1-receptor blockers [19,20]. Prophylactic or early treatment is feasible only in few clinical situations, such as known viral infection of the liver.…”

Section: Discussionmentioning

confidence: 94%

“…Different groups have previously investigated the effect of statins on hepatic inflammation [19], fibrosis [9,20,21], and also cirrhosis with portal hypertension [1,21,28]. They have shown beneficial effects on portal hypertension [1,28] and on angiotensin II-induced inflammation [19,20], but a significant effect on liver fibrosis and HSC in vivo has not been found to date [9,20,21].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Atorvastatin attenuates hepatic fibrosis in rats after bile duct ligation via decreased turnover of hepatic stellate cells

Trebicka

Hennenberg

Odenthal

et al. 2010

Journal of Hepatology

203

214

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Atorvastatin attenuates hepatic fibrosis in rats after bile duct ligation via decreased turnover of hepatic stellate cells

Trebicka

Hennenberg

Odenthal

et al. 2010

Journal of Hepatology

203

214

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“…188 However, adding a statin to candesartan can significantly enhance its suppressive effects on TGF-β1 expression and fibrogenesis. 189 Other agents, like valsartan 190 and irbesartan, 134 have been erratically evaluated in steatohepatitis, although presumably they will have similar effects to other available ARBs. As for the newer agents, we still await studies.…”

Section: Targeting the Ras In Nashmentioning

confidence: 99%

Angiotensin receptor blockers in the treatment of NASH/NAFLD: Could they be a first-class option?

Georgescu

2008

Adv Therapy

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Nonalcoholic fatty liver disease (NAFLD) is a condition pathogenically linked to metabolic syndrome (MS) by insulin resistance (IR), and characterized by hepatic steatosis in the absence of significant alcohol use, hepatotoxicity, and/or other known liver diseases.The principles of NAFLD therapy target IR: the key point of MS. As the renin-angiotensin system (RAS) plays a central role in IR, and subsequently in NAFLD and nonalcoholic steatohepatitis (NASH), an attempt to block the deleterious effects of RAS overexpression seems a logical target. While many potential therapies tested in NASH target only the consequences of this condition, or try to "get rid" of excessive fat, angiotensin receptor blockers (ARBs) could act as an elegant tool for adequate correction of the various imbalances that act in harmony in NASH/NAFLD. Indeed, by inhibiting RAS we can improve the intracellular insulin signaling pathway, better control adipose tissue proliferation and adipokine production, and produce more balanced local and systemic levels of various cytokines. At the same time, by controlling the local RAS in the liver we might be able to prevent at least fibrosis and also slow down the vicious cycle that links steatosis to necroinflammation. By targeting the pancreatic effects of angiotensin we should be able to preserve an adequate insulin secretion and acquire a better metabolic balance.In our opinion there are two major advantages of ARBs that make them a possible therapeutic option for treating NASH and MS: their specific antihypertensive effect, and their impact on liver fibrosis. In light of this, and based on the current evidence (including existent human studies), we can speculate that some ARBs like telmisartan, candesartan, and losartan can be beneficial in treating NASH/NAFLD and its consequences, and further larger controlled clinical trials will bring consistent data into this field.

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“…En pratique, nous recommandons, lorsqu'un patient avec fibrose hépa-tique significative reçoit un traitement pour HTA ne comportant pas de sartan, d'envisager une conversion vers un sartan (irbésartan). L'étape suivante sera de tester les associations ou les médicaments bloquant deux voies de signalisation comme l'association sartan et statine [23].…”

Section: Resultsunclassified

Médicaments ayant un effet sur la fibrose hépatique

Raimbault

Veillon

Oberti

et al. 2007

J Afr Hepato Gastroenterol

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La fibrose hépatique est consécutive à une fibrogenèse prolongée, au cours de laquelle on observe une fabrication excessive et un dépôt anarchique des composants de la matrice extracellulaire, en réponse à l'agression chronique du foie par divers agents. Parmi les voies de signalisation, l'angiotensine II (ATII) semble jouer un rôle majeur dans la fibrogenèse hépatique, car elle entraîne l'activation des cellules stellaires hépatiques, la sécrétion de cytokines pro-inflammatoires (dont le TGF-b1) et la synthèse de collagène par sa liaison aux récepteurs AT1. Plusieurs études montrent que les sartans ont des effets potentiellement intéressants sur la fibrose hépatique au cours de l'hépatite chronique C et de la NAFLD. Le développement de médicaments antifibrosants aurait un impact considérable sur la prise en charge des hépatopathies chroniques. Nous avons dressé une liste des médicaments, à partir d'études précliniques et cliniques, suggérant un effet pro-ou antifibrosant hépatique, en évaluant la pertinence clinique des effets pour chaque molécule.Abstract: Liver fibrosis is the result of excessive fibrogenesis secondary to miscellaneous injuries; thus, extracellular matrix accumulates within the liver. Among signalling pathways, angiotensin II (ATII) seems to play a major role. It induces the activation of stellate liver cells, the secretion of several pro-inflammatory cytokines (especially TGF-b1) and collagen synthesis after binding to AT1 receptors. Sartans are the main antagonists of AT1 receptors to ATII. Several studies have shown potentially interesting effects of sartans on liver fibrosis in chronic hepatitis C and NAFLD. The development of antifibrotic drugs would have a considerable impact on patient care in chronic liver diseases. We have listed pro-and antifibrotic drugs available on the market. The clinical relevance is evaluated for each drug.

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Pitavastatin Enhances the Anti-Fibrogenesis Effects of Candesartan, an Angiotensin Ⅱ Receptor Blocker, on CCl<sub>4</sub>-Induced Liver Fibrosis in Rats

Cited by 16 publications

References 4 publications

Atorvastatin attenuates hepatic fibrosis in rats after bile duct ligation via decreased turnover of hepatic stellate cells

Atorvastatin attenuates hepatic fibrosis in rats after bile duct ligation via decreased turnover of hepatic stellate cells

Angiotensin receptor blockers in the treatment of NASH/NAFLD: Could they be a first-class option?

Médicaments ayant un effet sur la fibrose hépatique

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