Редактирование: CREG1

Protein CREG1 precursor (Cellular repressor of E1A-stimulated genes 1) [CREG] [UNQ727/PRO1409]

==Publications==

{{medline-entry
|title=[[CREG1]] ameliorates myocardial fibrosis associated with autophagy activation and Rab7 expression.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25774384
|abstract=In cardiomyocytes subjected to stress, autophagy activation is a critical survival mechanism that preserves cellular energy status while degrading damaged proteins and organelles. However, little is known about the mechanisms that govern this autophagic response. Cellular repressor of E1A genes ([[CREG1]]) is an evolutionarily conserved lysosomal protein, and an important new factor in regulating tissues homeostasis that has been shown to antagonize injury of tissues or cells. In the present study, we aimed to investigate the regulatory role of [[CREG1]] in cardiac autophagy, and to clarify autophagy activation mechanisms. First, we generated a [[CREG1]] haploinsufficiency (Creg1( /-)) mouse model, and identified that [[CREG1]] deficiency aggravates myocardial fibrosis in response to aging or angiotensin II (Ang II). Conversely, exogenous infusion of recombinant [[CREG1]] protein complete reversed cardiac damage. CERG1 deficiency in Creg1( /-) mouse heart showed a market accumulation of autophagosome that acquired LC3II and beclin-1, and a decrease in autophagic flux clearance as indicated by upregulating the level of p62. Inversely, restoration of [[CREG1]] activates cardiac autophagy, Furthermore, chloroquine, an inhibitor of lysosomal acidification, was used to confirm that [[CREG1]] protected the heart tissue against Ang II-induced fibrosis by activating autophagy. Using adenoviral infection of primary cardiomyocytes, overexpression of [[CREG1]] with concurrent resveratrol treatment significantly increased autophagy, while silencing [[CREG1]] blocked the resveratrol-induced autophagy. These results suggest that [[CREG1]]-induced autophagy is required to maintain heart function in the face of stress-induced myocardiac damage. Both in vitro and in vivo studies identified that [[CREG1]] deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in [[CREG1]]-induced cardiomyocyte autophagy. These findings suggest that autophagy activation via [[CREG1]] may be a viable therapeutic strategy autophagy for improving cardiac performance under pathologic conditions. This article is part of a Special Issue entitled: autophagy and protein quality control in cardiometabolic diseases.
|mesh-terms=* Aging
* Angiotensin II
* Animals
* Autophagy
* Cells, Cultured
* Disease Susceptibility
* Fibrosis
* Lysosomes
* Male
* Mice
* Myocardium
* Myocytes, Cardiac
* Phagosomes
* Recombinant Proteins
* Repressor Proteins
* rab GTP-Binding Proteins

|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2014.05.027
}}