Fibrosis

Publication Title: 
Disease Models & Mechanisms

Cardiac fibrosis is critically involved in the adverse remodeling accompanying dilated cardiomyopathies (DCMs), which leads to cardiac dysfunction and heart failure (HF). Connective tissue growth factor (CTGF), a profibrotic cytokine, plays a key role in this deleterious process. Some beneficial effects of IGF1 on cardiomyopathy have been described, but its potential role in improving DCM is less well characterized.

Author(s): 
Touvron, Melissa
Escoubet, Brigitte
Mericskay, Mathias
Angelini, Aude
Lamotte, Luciane
Santini, Maria Paola
Rosenthal, Nadia
Daegelen, Dominique
Tuil, David
Decaux, Jean-FranÁois
Publication Title: 
PloS One

The immune response is essential for survival by destroying microorganisms and pre-cancerous cells. However, inflammation, one aspect of this response, can result in short- and long-term deleterious side-effects. Mclk1?/? mutant mice can be long-lived despite displaying a hair-trigger inflammatory response and chronically activated macrophages as a result of high mitochondrial ROS generation. Here we ask whether this phenotype is beneficial or simply tolerated. We used models of infection by Salmonella serovars and found that Mclk1?/?

Author(s): 
Wang, Dantong
Wang, Ying
Argyriou, Catherine
CarriËre, Audrey
Malo, Danielle
Hekimi, Siegfried
Publication Title: 
The Tohoku Journal of Experimental Medicine

Myocardial infarction (MI) leads to progressive left ventricular (LV) dilatation and is associated with interstitial fibrosis in the non-infarcted myocardium. The NF-?B signaling pathway plays an important role in ventricular remodeling after MI. Recent studies have indicated that the anti-malarial agent artemisinin can inhibit NF-?B activation, which may attenuate post-infarct myocardial remodeling. In this study, we investigated the effect of artemisinin on post-infarct myocardial remodeling using a rat model of MI.

Author(s): 
Gu, Yongwei
Wang, Xi
Wang, Xin
Yuan, Mingjie
Wu, Gang
Hu, Juan
Tang, Yanhong
Huang, Congxin
Publication Title: 
Liver International: Official Journal of the International Association for the Study of the Liver

BACKGROUND: Cholestasis is a common disease of the liver. Chronic cholestasis eventually leads to hepatic cirrhosis and fibrosis, and rodent chronic cholestasis models are used to study aspects of fibrosis and cirrhosis. Cholestasis-induced liver injury and fibrosis are associated with increased oxidative stress and inflammation. Few pharmacological therapies exist for treatment of cholestasis or cirrhosis, but it is known that humans with better nutritional intake are less likely to develop certain types of cirrhosis.

Author(s): 
Donepudi, Ajay C.
Aleksunes, Lauren M.
Driscoll, Maureen V.
Seeram, Navindra P.
Slitt, Angela L.
Publication Title: 
Liver International: Official Journal of the International Association for the Study of the Liver

BACKGROUND: Cholestasis is a common disease of the liver. Chronic cholestasis eventually leads to hepatic cirrhosis and fibrosis, and rodent chronic cholestasis models are used to study aspects of fibrosis and cirrhosis. Cholestasis-induced liver injury and fibrosis are associated with increased oxidative stress and inflammation. Few pharmacological therapies exist for treatment of cholestasis or cirrhosis, but it is known that humans with better nutritional intake are less likely to develop certain types of cirrhosis.

Author(s): 
Donepudi, Ajay C.
Aleksunes, Lauren M.
Driscoll, Maureen V.
Seeram, Navindra P.
Slitt, Angela L.
Publication Title: 
Acta Myologica: Myopathies and Cardiomyopathies: Official Journal of the Mediterranean Society of Myology / Edited by the Gaetano Conte Academy for the Study of Striated Muscle Diseases

Muscular dystrophies such as Duchenne muscular dystrophy (DMD) are usually approached as dysfunctions of the affected skeletal myofibres and their force transmission. Comparatively little attention has been given to the increase in connective tissue (fibrosis) which accompanies these muscular changes. Interestingly, an increase in endomysial tissue is apparent long before any muscular degeneration can be observed. Fibrosis is the result of a reactive or reparative process involving mechanical, humoral and cellular factors.

Author(s): 
Klingler, Werner
Jurkat-Rott, Karin
Lehmann-Horn, Frank
Schleip, Robert
Publication Title: 
Acta Myologica: Myopathies and Cardiomyopathies: Official Journal of the Mediterranean Society of Myology / Edited by the Gaetano Conte Academy for the Study of Striated Muscle Diseases

Muscular dystrophies such as Duchenne muscular dystrophy (DMD) are usually approached as dysfunctions of the affected skeletal myofibres and their force transmission. Comparatively little attention has been given to the increase in connective tissue (fibrosis) which accompanies these muscular changes. Interestingly, an increase in endomysial tissue is apparent long before any muscular degeneration can be observed. Fibrosis is the result of a reactive or reparative process involving mechanical, humoral and cellular factors.

Author(s): 
Klingler, Werner
Jurkat-Rott, Karin
Lehmann-Horn, Frank
Schleip, Robert
Publication Title: 
The Journal of Biological Chemistry

The roles of MEK, ERK, the epsilon and alpha isoforms of protein kinase C (PKC), and caveolin-1 in regulating collagen expression were studied in normal lung fibroblasts. Knocking down caveolin-1 gave particularly striking results. A 70% decrease caused a 5-fold increase in MEK/ERK activation and collagen expression. The combined data reveal a branched signaling pathway. In its central portion MEK activates ERK, leading to increased collagen expression. Two branches converge on MEK/ERK. In one, increased PKCepsilon leads to MEK/ERK activation.

Author(s): 
Tourkina, Elena
Gooz, Pal
Pannu, Jaspreet
Bonner, Michael
Scholz, Dimitri
Hacker, Sharon
Silver, Richard M.
Trojanowska, Maria
Hoffman, Stanley
Publication Title: 
PloS One

BACKGROUND: Fibulin-4 is an extracellular matrix protein expressed by vascular smooth muscle cells that is essential for maintaining arterial integrity. Fibulin-4(-/-) mice die just before birth due to arterial hemorrhage, but fibulin-4(+/-) mice appear to be outwardly normal. Experiments were therefore performed to determine whether fibulin-4(+/-) mice display arterial pathologies on a microscopic scale.

Author(s): 
Cudilo, Elizabeth
Al Naemi, Hamda
Marmorstein, Lihua
Baldwin, Ann L.
Publication Title: 
The American Journal of Pathology

In diabetes and hypertension, the induction of increased transforming growth factor-beta (TGF-beta) activity due to glucose and angiotensin II is a significant factor in the development of fibrosis and organ failure. We showed previously that glucose and angiotensin II induce the latent TGF-beta activator thrombospondin-1 (TSP1).

Author(s): 
Belmadani, Souad
Bernal, Juan
Wei, Chih-Chang
Pallero, Manuel A.
Dell'italia, Louis
Murphy-Ullrich, Joanne E.
Berecek, Kathleen H.

Pages

Subscribe to RSS - Fibrosis