Deciphering Fibrosis: Drivers of Fibrotic Disease in the Liver and Heart скачать в хорошем качестве

Deciphering Fibrosis: Drivers of Fibrotic Disease in the Liver and Heart

Participating Experts: Scott L. Friedman, MD (Mount Sinai Hospital) and Douglas E. Vaughan MD (Northwestern) ⬇️ Expand “Show More” to view abstract and table of contents Download the Mechanisms of Fibrosis Pathway: https://cst-science.com/pp1ikv Fibrotic diseases of the heart and liver impact a significant portion of the global population and are a growing public health concern. Fibrosis occurs when fibroblasts deposit excess extracellular material within the tissue in response to certain stimuli or injury. Myocardial fibrosis is associated with nearly all forms of heart disease. The pathological changes that can result from fibrosis include cardiomyocyte hypertrophy, chamber dilation, heart valve stiffening, and others, all of which contribute to heart failure. Nonalcoholic steatohepatitis (NASH) is a fatty liver disease characterized by hepatocyte inflammation that contributes to fibrosis, cirrhosis, and liver failure. NASH is closely linked to obesity and diabetes; changes in diet have thus contributed to its expansion and impact across the globe. Understanding the underlying biology of fibrosis is critical for the diagnosis, treatment, and management of cardiac fibrosis, NASH, and other fibrotic diseases. Table of Contents 0:25 Welcome and overview 2:46 Scott Friedman speaker profile 3:56 Fibrosis accounts for ~45% of all deaths in industrialized nations 5:46 Fibrosis is a common pathway among different etiologies of liver disease 6:38 NAFLD spectrum of hepathic pathology 8:38 Prognostic implications of NAFLD vs NASH 10:48 HCC development in western diet/CCI4 NASH Model 12:22 Core vs. regulatory pathways in liver fibrosis 13:53 Systemic regulators of Fibrosis in NASH 15:22 Hepatic Stellate cell activation – a central event in liver fibrosis 19:49 Fibrosis regression after 240 weeks of Hepatitis B viral suppression 20:37 Mechanisms of Fibrosis Reversibility: Enzymes and Cellular Sources 22:16 NASH Fibrosis Summary 23:36 Douglas Vaughan speaker profile 24:23 Spontaneous cardiac fibrosis in PAI-1 deficient mice and men: a rare mutation informs a common molecular pathophysiology 25:39 Cardiac fibrosis: scope of the problem 26:51 The Plasminogen Activator system: myriad functions in extracellular proteolysis 29:27 Cardiac fibrosis in humans with complete PAI-1 deficiency 31:39 Age-dependent and cardiac-specific fibrosis in PAI-1 / mice 33:46 Cardiomyocytes synthesize TGF-β in AngII-treated hearts in vivo 35:04 PAI-1 overexpression suppresses TGF-β production by hiPSC-CMs 37:02 PAI-1 regulates early AngII-mediated cardiac hypertrophy and transcriptional events 38:28 Enhanced fibrosis in the PAI-1 / is inhibited by co-administration of BMP-7 40:41 Summary 43:31 Questions and answers About CST®: Cell Signaling Technology (CST) is a private, family-owned company, founded by scientists and dedicated to providing high-quality research tools to the biomedical research community. Our employees operate worldwide from our U.S. headquarters in Massachusetts, and our offices in the Netherlands, China, and Japan. https://cellsignal.com/about Cell Signaling Technology and CST are registered trademarks of Cell Signaling Technology, Inc. All other trademarks are the property of their respective owners. #antibody #CSTWebinar