scispace - formally typeset
J

Juan Armendáriz-Borunda

Researcher at University of Guadalajara

Publications -  190
Citations -  4211

Juan Armendáriz-Borunda is an academic researcher from University of Guadalajara. The author has contributed to research in topics: Fibrosis & Cirrhosis. The author has an hindex of 34, co-authored 161 publications receiving 3539 citations. Previous affiliations of Juan Armendáriz-Borunda include Monterrey Institute of Technology and Higher Education & Veterans Health Administration.

Papers
More filters
Journal ArticleDOI

A pentapeptide from type I procollagen promotes extracellular matrix production.

TL;DR: It is postulate that the extracellular matrix production in fibroblasts may be subject to either positive or negative feedback regulation depending on the repertoire of specific proteases during postinflammatory tissue regeneration and fibrosis.
Journal ArticleDOI

Pirfenidone effectively reverses experimental liver fibrosis

TL;DR: This new drug might be useful in healing human disease and reduce hepatic fibrosis in rats experimentally induced by chronic administration of CCl(4) and bile-duct ligation.
Journal ArticleDOI

Treatment with human metalloproteinase-8 gene delivery ameliorates experimental rat liver cirrhosis.

TL;DR: In this paper, an extrahepatic human neutrophil collagenase complementary DNA (matrix metalloprotease-8) cloned in an adenovirus vector was used as a therapeutic agent in cirrhosis.
Journal ArticleDOI

The multifaceted role of pirfenidone and its novel targets

TL;DR: There is a growing understanding of the molecular effects of PFD on the wound healing mechanism, leading to novel approaches for the management of fibrosis in lung, liver and renal tissues, and it is possible that combined therapeutic regimens that include this wide-application molecule, pirfenidone, could offer a useful treatment for fibrotic disease.
Journal ArticleDOI

Liver cirrhosis is reverted by urokinase-type plasminogen activator gene therapy.

TL;DR: In a rat cirrhosis model, a single iv administration of a replication-deficient adenoviral vector encoding a nonsecreted form of human uPA resulted in high production of functional uPA protein in the liver, which led to induction of collagenase expression and reversal of fibrosis with concomitant hepatocyte and improved liver function.