Cardiac Fibrosis
Cardiac Fibrosis - Related Videos
02:49
Picrosirius Red Polarization Staining: A Technique To Detect Fibrosis in Cardiac Tissue Sections Using Bright-Field Microscopy
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2025
This video describes the picrosirius red staining of fibrotic tissues to detect excessive collagen deposition in fibrotic tissue sections. The staining technique helps assess collagen expression in connective-tissue diseases.
09:44
Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
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2025
This protocol demonstrates how the Src homology 2 domain-containing 5'-inositol phosphatase (SHIP)-deficient mouse model of Crohn disease (CD)-like ileal inflammation and fibrosis can be used to test novel therapeutics for CD.
07:31
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
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Cited by 26 •
2016
A rat model of abdominal aortic constriction that induces cardiac hypertrophy and remodeling is described. An efficient, highly-reproducible, and minimally-invasive method is used to provide a simple yet useful platform for research in myocardial hypertrophy and dysfunction.
08:25
Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling
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Cited by 11 •
2015
Streptococcus pneumoniae forms discrete non-purulent microscopic lesions in the heart. Outlined is the protocol for a murine model of cardiac microlesion formation. Instruction is provided on microlesion visualization using microscopy, discrimination between early and late microlesions, and methods to detect cardiac remodeling in hearts of convalescent animals.
09:27
The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
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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.
FAQs
Following cardiac injury or persistent stress, inflammatory and neurohormonal signals activate cardiac fibroblasts. These cells then produce and deposit extracellular matrix proteins, including collagen. Fibrosis becomes more pronounced when matrix breakdown does not adequately balance new matrix production, allowing tissue accumulation that alters myocardial stiffness and can progressively impair cardiac performance.
Accumulated collagen changes the myocardial environment in two important ways. By stiffening the heart muscle, it can reduce relaxation during the cardiac cycle. The remodeled tissue can also disrupt normal electrical conduction, creating conditions associated with arrhythmias. Thus, matrix accumulation influences both mechanical function and electrical stability rather than affecting structure alone.
Progression reflects the interaction between ongoing injury or persistent stress, fibroblast activation, extracellular matrix deposition, and matrix breakdown. Continued inflammatory or neurohormonal signaling can sustain fibroblast activity, while inadequate removal of deposited matrix favors accumulation. The resulting remodeling may become clinically important when it stiffens the myocardium or interferes with electrical conduction.
The consequences depend on how remodeling alters cardiac tissue. Increased stiffness can limit relaxation and impair overall cardiac function, contributing to heart failure. At the same time, disruption of electrical conduction can promote abnormal rhythms. These linked mechanical and electrical effects help explain why fibrosis is relevant to multiple cardiovascular disease outcomes.
Clinical research evaluates fibrosis through complementary approaches, including imaging, tissue analysis, and circulating biomarkers. Imaging can support assessment in the heart, tissue analysis examines structural changes directly, and circulating biomarkers provide measurable signals related to disease processes. Using these approaches helps researchers investigate fibrosis for risk stratification and disease monitoring.
Assessment is particularly relevant in cardiovascular diseases where injury or persistent stress may drive myocardial remodeling. Information from imaging, tissue analysis, or circulating biomarkers can help characterize risk and monitor changes over time. In research, these measurements also support evaluation of whether disease-related remodeling is progressing or responding to an intervention.
Therapeutic research focuses on mechanisms that sustain remodeling, especially cardiac fibroblast activation and extracellular matrix turnover. Investigators may therefore evaluate approaches designed to reduce fibroblast activation or modify matrix remodeling. The rationale is to limit excessive tissue accumulation, preserve myocardial relaxation and conduction, and potentially reduce fibrosis-related cardiovascular complications.