Retrospective analysis of the morphofunctional architectonics and pathohistological transformation of the myocardium: from the molecular norm to regenerative potential in remodelling and ischaemia (literature review)
DOI:
https://doi.org/10.26641/1997-9665.2026.2.5-11Keywords:
myocardium, histological architecture, ischemia, myocardial infarction, immunohistochemistry.Abstract
Introduction. Myocardial viability depends on the spatial organization of subcellular structures (ion clusters, nanodomains), whose disorganization of which causes rhythm disturbances even before the appearance of histological signs of necrosis. This makes an in-depth study of cardiac microarchitecture critically important for clinical practice. Aim. To systematize modern histological, ultrastructural, and immunohistochemical criteria for evaluating the myocardium in normal conditions, during adaptive remodeling, ischemia, and inflammation, as well as to analyze the regenerative potential of the tissues. Methods. A systematic review was conducted, resulting in the selection of 25 sources from the PubMed, Scopus, and Web of Science databases spanning 1990–2026 (with a focus on the last 5 years) using the keywords: myocardium, histology, pathology. Results. Normal myocardial architecture is maintained by intercalated discs and ankyrins, which serve as molecular "anchors" for ion channels. During hypoxia, ankyrin proteolysis disrupts this stability. In ischemia, ultrastructural changes (mitochondrial swelling) are recorded as early as 30 minutes. For the ultra-early verification of true ischemia and necrosis, specific immunohistochemical markers (C9 complex, SIRT1) are utilized, and the local tissue loss of troponin C is monitored. Post-necrotic remodeling culminates in irreversible collagen scarring involving myofibroblasts (α-SMA expression). Surviving muscle "bridges" within the scar can generate arrhythmias. Simultaneously, regeneration faces the connexin-43 (Cx43) paradox: although differentiated progenitor cells express it, the excessive extracellular matrix physically isolates cardiomyocytes, blocking electrical contacts. Conclusion. The early verification of ischemia and inflammation relies on electron microscopy and specific markers (C9, CD3). Overcoming barriers in regenerative medicine requires comprehensive histomatrix analysis to combat fibrosis and restore conduction.
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