Activin or Follistatin: Which is More Beneficial to Support Liver Regeneration After Massive Hepatectomy?

Endo, Daisuke; Makuuchi, Masatoshi; Kojima, Itaru

doi:10.1507/endocrj.53.73

Cited by 29 publications

(22 citation statements)

References 17 publications

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“…Following partial hepatectomy follistatin expression was up-regulated after 24-48 h, the time period in which hepatocyte replication was increased [50] . Under similar conditions administration of follistatin accelerated liver regeneration but led to impaired restoration of normal tissue architecture and compromised liver function [108][109][110] . Administration of exogenous follistatin in CCl4 treated rats attenuated the formation of liver fibrosis [111] .…”

Section: Follistatinmentioning

confidence: 97%

Activins and activin antagonists in hepatocellular carcinoma

Deli

Kreidl²,

Santifaller³

et al. 2008

WJG

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Section: Follistatinmentioning

confidence: 97%

Activins and activin antagonists in hepatocellular carcinoma

Deli

Kreidl²,

Santifaller³

et al. 2008

WJG

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“…Following partial hepatectomy, follistatin expression was up-regulated after 24-48 h, the time period in which hepatocyte replication was increased [42] . Administration of exogenous follistatin after partial hepatectomy accelerated liver regeneration but led to impaired restoration of normal tissue architecture and compromised liver function [122][123][124] . Administration of follistatin in CCl4-treated rats attenuated the formation of liver fibrosis [125] .…”

Section: Follistatinmentioning

confidence: 99%

Activins and follistatins: Emerging roles in liver physiology and cancer

Kreidl

Öztürk²,

Metzner³

et al. 2009

WJH

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Activins are secreted proteins belonging to the TGF-β family of signaling molecules. Activin signals are crucial for differentiation and regulation of cell proliferation and apoptosis in multiple tissues. Signal transduction by activins relies mainly on the Smad pathway, although the importance of crosstalk with additional pathways is increasingly being recognized. Activin signals are kept in balance by antagonists at multiple levels of the signaling cascade. Among these, follistatin and FLRG, two members of the emerging family of follistatin-like proteins, can bind secreted activins with high affinity, thereby blocking their access to cell surface-anchored activin receptors. In the liver, activin A is a major negative regulator of hepatocyte proliferation and can induce apoptosis. The functions of other activins expressed by hepatocytes have yet to be more clearly defined. Deregulated expression of activins and follistatin has been implicated in hepatic diseases including inflammation, fibrosis, liver failure and primary cancer. In particular, increased follistatin levels have been found in the circulation and in the tumor tissue of patients suffering from hepatocellular carcinoma as well as in animal models of liver cancer. It has been argued that up-regulation of follistatin protects neoplastic hepatocytes from activin-mediated growth inhibition and apoptosis. The use of follistatin as biomarker for liver tumor development is impeded, however, due to the presence of elevated follistatin levels already during preceding stages of liver disease. The current article summarizes our evolving understanding of the multi-faceted activities of activins and follistatins in liver physiology and cancer.

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“…Activin A is an autocrine inhibitor of hepatocytes and functions to maintain constant liver mass, and follistatin may be useful to promote liver regeneration and increase the liver mass. It is of note that excessive stimulation of hepatocyte growth is not beneficial [20]. Follistatin should be used appropriately to promote liver regeneration.…”

Section: Livermentioning

confidence: 99%