Myocardial degeneration
Overview
Post-infarction myocardial fibrosis is a pathological process characterized by the replacement of necrotic cardiac muscle areas with connective (scar) tissue that develops following a myocardial infarction.
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Myocardial infarction occurs as a result of an acute disruption of blood supply to the myocardium, primarily caused by:
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Thrombosis of an atherosclerotic plaque in a coronary artery;
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Severe coronary artery spasm (less common).
Biological Processes and Key Morphological Changes
As a consequence of chronic or acute ischemia, a region of the myocardium becomes deprived of oxygen, leading to cardiomyocyte death and the initiation of the fibrotic repair process.
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Within the necrotic area, a cascade of inflammatory responses is activated, involving neutrophils, macrophages, and other immune cells responsible for clearing necrotic debris.
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Following the acute inflammatory phase, granulation tissue begins to form. This stage is characterized by the appearance of new blood vessels, activated fibroblasts, and active collagen deposition.
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Over time, the granulation tissue gradually transforms into mature fibrous tissue through continued collagen synthesis and the reorganization of extra- and intracellular structures.
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The final stage of this process is post-infarction cardiosclerosis - a dense collagenous scar that provides structural stability to the myocardium but lacks contractile function.
Project Strategy
The project aims to develop a multi-stage therapeutic product designed to address the core biological mechanisms of post-infarction myocardial fibrosis.
The therapeutic approach is organized into the following stages:
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Acute immune regulation and cardiomyocyte protection
Modulation of post-infarction inflammation and stabilization of viable cardiomyocytes in the infarct border zone to prevent secondary damage and prepare tissue for repair. -
Controlled clearance of necrotic tissue and initiation of regeneration
Activation of immune and cellular mechanisms to ensure precise removal of necrotic structures and stimulation of endogenous cardiomyocyte regeneration. -
Complete regeneration and functional myocardial remodeling
Promotion of new cardiomyocyte formation, restoration of vascular integrity, and structural reorganization of myocardial tissue to achieve functional recovery.