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Autophagy and autophagins

Título: Autophagy and autophagins
Descripción: With the generation of autophagin-1/Atg4B-deficient mice, recently reported, we have progressed in our attempt to identify the in vivo physiological and pathological roles of autophagins

Autophagy and colitis

Título: Autophagy and Colitis
Descripción: Here, we describe autophagy-related 4B, cysteine peptidase/autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis.

Autophagy and equilibrioception

Título: Autophagy and equilibrioception
Descripción: , Atg4b-null mice showed defects in the development of otoconia, organic calcium carbonate crystals essential for sense of balance (equilibrioception).

Autophagy and longevity

Título: Autophagy and longevity
Descripción: Here we investigated the differences and similarities in spermidine and resveratrol-induced autophagy. The deacetylase sirtuin 1 (SIRT1) and its orthologs are required for the autophagy induction.

Autophagy and Lung Fibrosis

Título: Autophagy and Lung Fibrosis
Descripción: ATG4B protease and autophagy play a crucial role protecting epithelial cells against bleomycin-induced stress and apoptosis, and in the regulation of the inflammatory and fibrotic responses.

Autophagy spermidine and resveratrol

Título: Autophagy spermidine and resveratrol
Descripción: these article underscore the importance of an autophagy regulatory network of antagonistic deacetylases and acetylases that can be pharmacologically manipulated.

Gelatinase B and Lung Fibrosis

Título: Gelatinase B and Lung Fibrosis
Descripción: we demonstrated that MMP9 degraded IGFBP-3 into lower molecular mass fragments. These findings suggest that increased activity of MMP9 secreted by alveolar macrophages in the lung microenvironment may have an antifibrotic effect

Gene expression in experimental lung fibrosis

Título: Gene expression in experimental lung fibrosis
Descripción: Lung fibrosis is the final result of a large number of disorders and is usually considered an irreversible process. In this study we aimed to document the time-related reversibility of bleomycin-induced lung fibrosis and to examine the gene expression profile.

Lung fibrosis animal model

Título: Lung fibrosis animal model
Descripción: The cytotoxic effect of bleomycin is dose–dependent and involves pneumonitis that proceeds to lung fibrosis (LF). Alveolar epithelial cells are the main target of bleomycin induced injury.

MMP Evolution

Título: MMP Evolution
Descripción: genomic studies of MMPs, including functional analysis of gene regulation and generation of novel animal models will help to answer the multiple questions still open in relation to a family of enzymes which strongly influence multiple events in life and disease.

MMP19 and Lung Fibrosis

Título: MMP19 Is a Key Regulator of Lung Fibrosis
Descripción: Up-regulation of MMP19 induced by lung injury may play a protective role in the development of fibrosis through the induction of PTGS2.Mmp19(-/-) mice showed a significantly increased lung fibrotic response to bleomycin compared with WT mice.

MMP8 and lung fibrosis

Título: MMP8 and lung fibrosis
Descripción: Mmp8(-/-) mice developed less fibrosis than their wildtype counterparts. This was related to an increase in lung inflammatory cells, MMP-9 and IL-10 levels in these mutant animals.

MMP8 and Lung Injury

Título: MMP8 and Lung Injury
Descripción: MMP-8 promotes acute inflammation after ventilation with high pressures, and its short-term inhibition could be a therapeutic goal to limit VILI

TIMPS and Lung Fibrosis

Título: TIMPS and Lung Fibrosis
Descripción: We evaluated the presence of tissue inhibitor of metalloproteinase (TIMP)-1, -2, -3, and -4; collagenase-1, -2, and -3; gelatinases A and B; and membrane type 1 matrix metalloproteinase (MMP) in 12 IPF and 6 control lungs.

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Hecho en México - Universidad Nacional Autónoma de México (UNAM) todos los derechos reservados 2012-2014 Sitio realizado por la Dirección General de Cómputo y de Tecnologías de Información y Comunicación (DGTIC). Esta página puede ser reproducida con fines no lucrativos, siempre y cuando se cite la fuente completa y su dirección electrónica, y no se mutile. De otra forma requiere permiso previo por escrito de la institución.

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