Alpha 2.0
Login Register
» Authors » Ignacio Montorfano

Ignacio Montorfano

Explore the profile of Ignacio Montorfano including associated specialties, affiliations and a list of published articles. Areas
Snapshot
Articles 11
Citations 229
Followers 0
Related Specialties
Biochemistry
Cell Biology
Molecular Biology
Top 10 Co-Authors
Felipe Simon
Cesar Echeverria
Claudio Cabello-Verrugio
Ricardo Armisen
Alvaro Becerra
Claudia Riedel
Pablo Tapia
Daniela Sarmiento
Diego Varela
Ricardo Fernandez
Published In
Infect Immun
Antioxid Redox Signal
PLoS One
Int J Biochem Cell Biol
Biometals
Affiliations
Soon will be listed here.
Recent Articles
1.
The characterization of anti-T. cruzi activity relationships between ferrocenyl, cyrhetrenyl complexes and ROS release
Echeverria C, Romero V, Arancibia R, Klahn H, Montorfano I, Armisen R, et al.
Biometals . 2016 Jul; 29(4):743-9. PMID: 27460450
Trypanosoma cruzi (T. cruzi) is the parasite that causes Chagas disease. Nifurtimox is the most used drug against the T. cruzi, this drug increases intermediaries nitro group, being mainly responsible...
2.
Chalcone-Induced Apoptosis through Caspase-Dependent Intrinsic Pathways in Human Hepatocellular Carcinoma Cells
Ramirez-Tagle R, Escobar C, Romero V, Montorfano I, Armisen R, Borgna V, et al.
Int J Mol Sci . 2016 Feb; 17(2):260. PMID: 26907262
Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers worldwide. Chemoprevention of HCC can be achieved through the use of natural or synthetic compounds that reverse, suppress or...
3.
Correction for Echeverría et al., Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2
Echeverria C, Montorfano I, Tapia P, Riedel C, Cabello-Verrugio C, Simon F
Infect Immun . 2016 Jan; 84(2):609-10. PMID: 26810751
No abstract available.
4.
Suppression of transient receptor potential melastatin 4 expression promotes conversion of endothelial cells into fibroblasts via transforming growth factor/activin receptor-like kinase 5 pathway
Echeverria C, Montorfano I, Cabello-Verrugio C, Armisen R, Varela D, Simon F
J Hypertens . 2015 Apr; 33(5):981-92. PMID: 25909699
Objective: To study whether transient receptor potential melastatin 4 (TRPM4) participates in endothelial fibrosis and to investigate the underlying mechanism. Methods: Primary human endothelial cells were used and pharmacological and...
5.
Endotoxin-induced vascular endothelial cell migration is dependent on TLR4/NF-κB pathway, NAD(P)H oxidase activation, and transient receptor potential melastatin 7 calcium channel activity
Sarmiento D, Montorfano I, Caceres M, Echeverria C, Fernandez R, Cabello-Verrugio C, et al.
Int J Biochem Cell Biol . 2014 Aug; 55:11-23. PMID: 25130439
Endothelial dysfunction is decisive and leads to the development of several inflammatory diseases. Endotoxemia-derived sepsis syndrome exhibits a broad inflammation-induced endothelial dysfunction. We reported previously that the endotoxin, lipopolysaccharide (LPS),...
6.
Oxidative stress mediates the conversion of endothelial cells into myofibroblasts via a TGF-β1 and TGF-β2-dependent pathway
Montorfano I, Becerra A, Cerro R, Echeverria C, Saez E, Morales M, et al.
Lab Invest . 2014 Jul; 94(10):1068-82. PMID: 25068653
During the pathogenesis of systemic inflammation, reactive oxygen species (ROS) circulate in the bloodstream and interact with endothelial cells (ECs), increasing intracellular oxidative stress. Although endothelial dysfunction is crucial in...
7.
Endotoxin-induced endothelial fibrosis is dependent on expression of transforming growth factors β1 and β2
Echeverria C, Montorfano I, Tapia P, Riedel C, Cabello-Verrugio C, Simon F
Infect Immun . 2014 Jun; 82(9):3678-86. PMID: 24935972
During endotoxemia-induced inflammatory disease, bacterial endotoxins circulate in the bloodstream and interact with endothelial cells (ECs), inducing dysfunction of the ECs. We previously reported that endotoxins induce the conversion of...
8.
Endotoxin induces fibrosis in vascular endothelial cells through a mechanism dependent on transient receptor protein melastatin 7 activity
Echeverria C, Montorfano I, Hermosilla T, Armisen R, Velasquez L, Cabello-Verrugio C, et al.
PLoS One . 2014 Apr; 9(4):e94146. PMID: 24710004
The pathogenesis of systemic inflammatory diseases, including endotoxemia-derived sepsis syndrome, is characterized by endothelial dysfunction. It has been demonstrated that the endotoxin lipopolysaccharide (LPS) induces the conversion of endothelial cells...
9.
Increases in reactive oxygen species enhance vascular endothelial cell migration through a mechanism dependent on the transient receptor potential melastatin 4 ion channel
Sarmiento D, Montorfano I, Cerda O, Caceres M, Becerra A, Cabello-Verrugio C, et al.
Microvasc Res . 2014 Feb; 98:187-96. PMID: 24518820
A hallmark of severe inflammation is reactive oxygen species (ROS) overproduction induced by increased inflammatory mediators secretion. During systemic inflammation, inflammation mediators circulating in the bloodstream interact with endothelial cells...
10.
Lipopolysaccharide induces a fibrotic-like phenotype in endothelial cells
Echeverria C, Montorfano I, Sarmiento D, Becerra A, Nunez-Villena F, Figueroa X, et al.
J Cell Mol Med . 2013 May; 17(6):800-14. PMID: 23635013
Endothelial dysfunction is crucial in endotoxaemia-derived sepsis syndrome pathogenesis. It is well accepted that lipopolysaccharide (LPS) induces endothelial dysfunction through immune system activation. However, LPS can also directly generate actions...