Ventricular Fibrosis
Ventricular Fibrosis - Related Videos
02:37
Surgical Aortic Debanding: A Procedure to Study Left Ventricular Reverse Remodeling in Murine Model of Aortic Constriction
0 Views •
2025
This video demonstrates the technique of aortic debanding, which can lead to reverse remodeling to limit the progression towards heart failure in a murine model. Post debanding, a significant reduction of ventricular afterload triggers regression of ventricular hypertrophy and fibrosis, causing a recovery in cardiac function.
09:27
The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
0 Views •
Cited by 11 •
2016
We describe a method to produce an animal model of liver fibrosis in the rat, and assess the degree of fibrosis by histological examination of the liver. The model can be used to study the development of liver disease as well as to test the efficacy of potential anti-fibrotic agents.
08:49
Use of Two Intracorporeal Ventricular Assist Devices As a Total Artificial Heart
0 Views •
Cited by 4 •
2018
Here, we present a protocol using two centrifugal pumps as a total artificial heart replacement.
01:23
Cystic Fibrosis: Pathogenesis
0 Views •
2024
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body. CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
06:26
Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
0 Views •
Cited by 1 •
2025
Mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD) with metabolic dysfunction, hepatic gene expression changes, and liver histopathological alterations that resemble human MASLD, including fibrosis that progresses to advanced fibrosis stage 3. This model can be used in studies of MASLD pathophysiology and in pre-clinical studies of new therapies.
FAQs
Persistent injury, inflammation, pressure overload, and related stressors can activate cardiac fibroblasts. Once activated, these cells produce and deposit excess extracellular matrix proteins, particularly collagen-rich material. Continued activity progressively changes the ventricular tissue environment, replacing healthier myocardium with scar tissue and linking fibroblast behavior to structural remodeling and declining cardiac performance.
Excess matrix alters the organization and physical properties of ventricular tissue. As scar tissue accumulates, the ventricle may become less compliant, limiting its ability to accommodate blood normally. Fibrotic remodeling can also interfere with electrical conduction through the myocardium, creating conditions that contribute to abnormal rhythms as well as impaired cardiac function.
Several forms of persistent cardiac stress can promote progression, including ongoing myocardial injury, inflammation, and pressure overload. These conditions maintain signals that activate fibroblasts and encourage extracellular matrix deposition. The resulting remodeling can become part of a continuing disease process, because increasing scar formation further disrupts ventricular structure and function.
Researchers examine ventricular fibrosis as a marker and mechanism of cardiac remodeling. Its extent can help connect underlying myocardial injury with changes in tissue structure, compliance, electrical conduction, and overall function. Studying these relationships supports efforts to identify biomarkers that reflect disease progression and to determine whether an intervention changes the fibrotic process.
Therapeutic studies can focus on several targets supported by the biology of fibrosis: cardiac fibroblast activation, extracellular matrix deposition, or the underlying causes of myocardial injury. Evaluating these targets helps determine whether limiting fibroblast activity or matrix accumulation can reduce adverse remodeling. It also allows researchers to distinguish treatments aimed at fibrosis from those addressing its initiating stressors.
Ventricular fibrosis provides a biological link between chronic cardiac stress and important disease outcomes. Structural remodeling can reduce ventricular compliance and disrupt conduction, while progressive replacement of healthy myocardium can impair cardiac performance. For this reason, fibrosis research contributes to understanding how heart failure and arrhythmias develop and supports biomarker and treatment investigations.