ArticleJournal of cellular and molecular medicine2009
Cellular repressor of E1A-stimulated genes attenuates cardiac hypertrophy and fibrosis.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- Hepatocyte cellular repressor of E1A-stimulated genes 1 protects against acetaminophen-induced liver injury by promoting autophagy.Acta pharmacologica Sinica · 2025Article
- Novel roles for CREG1 in hematopoiesis revealed by single-cell RNA sequencing.Cell & bioscience · 2025Article
- Integrated multi-omic high-throughput strategies across-species identified potential key diagnostic, prognostic, and therapeutic targets for atherosclerosis under high glucose conditions.Molecular and cellular biochemistry · 2025Article
- The role of CREG1 in megakaryocyte maturation and thrombocytopoiesis.International journal of biological sciences · 2023Article
- Hepatocyte-specific deletion of cellular repressor of E1A-stimulated genes 1 exacerbates alcohol-induced liver injury by activating stress kinases.International journal of biological sciences · 2022Article
- Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule.Computational and structural biotechnology journal · 2022Review
- Effects of CREG1 on Age-Associated Metabolic Phenotypes and Renal Senescence in Mice.International journal of molecular sciences · 2021Article
- The secreted inhibitor of invasive cell growth CREG1 is negatively regulated by cathepsin proteases.Cellular and molecular life sciences : CMLS · 2021Article
- The Structure and Biological Function of CREG.Frontiers in cell and developmental biology · 2018Review
- CREG1 heterozygous mice are susceptible to high fat diet-induced obesity and insulin resistance.PloS one · 2017Article
- Achievement of a target dose of bisoprolol may not be a preferred option for attenuating pressure overload-induced cardiac hypertrophy and fibrosis.Experimental and therapeutic medicine · 2016Article
- Fn14 is regulated via the RhoA pathway and mediates nuclear factor-kappaB activation by Angiotensin II.American journal of translational research · 2016Article
- Drosophila melanogaster cellular repressor of E1A-stimulated genes is a lysosomal protein essential for fly development.Biochimica et biophysica acta · 2014Article
- Inhibition of farnesyl pyrophosphate synthase prevents angiotensin II-induced cardiac fibrosis in vitro.Clinical and experimental immunology · 2014Article
- Identifying and mapping cell-type-specific chromatin programming of gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Cellular repressor of E1A stimulated genes enhances endothelial monolayer integrity.Molecular biology reports · 2013Article
- Cardiac-specific mindin overexpression attenuates cardiac hypertrophy via blocking AKT/GSK3β and TGF-β1-Smad signalling.Cardiovascular research · 2011Article
- CREG1 enhances p16(INK4a) -induced cellular senescence.Cell cycle (Georgetown, Tex.) · 2011Article
- Tetrandrine blocks cardiac hypertrophy by disrupting reactive oxygen species-dependent ERK1/2 signalling.British journal of pharmacology · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular repressor of E1A-stimulated genes (CREG) is a secreted glycoprotein of 220 amino acids. It has been proposed that CREG acts as a ligand that enhances differentiation and/or reduces cell proliferation. CREG has been shown previously to attenuate cardiac hypertrophy in vitro. However, such a role has not been determined in vivo. In the present study, we tested the hypothesis that overexpression of CREG in the murine heart would protect against cardiac hypertrophy and fibrosis in vivo. The effects of constitutive human CREG expression on cardiac hypertrophy were investigated using both in vitro and in vivo models. Cardiac hypertrophy was produced by aortic banding and infusion of angiotensin II in CREG transgenic mice and control animals. The extent of cardiac hypertrophy was quantitated by two-dimensional and M-mode echocardiography as well as by molecular and pathological analyses of heart samples. Constitutive over-expression of human CREG in the murine heart attenuated the hypertrophic response, markedly reduced inflammation. Cardiac function was also preserved in hearts with increased CREG levels in response to hypertrophic stimuli. These beneficial effects were associated with attenuation of the mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase 1 (MEK-ERK1)/2-dependent signalling cascade. In addition, CREG expression blocked fibrosis and collagen synthesis through blocking MEK-ERK1/2-dependent Smad 2/3 activation in vitro and in vivo. Therefore, the expression of CREG improves cardiac functions and inhibits cardiac hypertrophy, inflammation and fibrosis through blocking MEK-ERK1/2-dependent signalling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.