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)
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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
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