Morphometric, Histopathological, and Immunohistochemical Evaluation of Myocardial Remodeling in Cisplatin-Induced Renal Failure in Rats
Kosimov Umid Usmonovich Doctor of the pediatric intensive care unit of the Bukhara branch of the Scientific Center for Emergency Medical Care of the Republic of Uzbekistan. 0009-0000-1298-2329
Turniyozov Azamat AskarovichHead of the Cardiology Department of the Republican Scientific Center for Emergency Medical Care of the Navoi Branch (Navoi, Republic of Uzbekistan). https://orcid.org/0009-0007-5246-3698
Bakhronov Jurat DjurakulovichDoctor of Medical Sciences, Professor, Head of the Department of Histology, Cytology and Embryology of the Bukhara Medical Institute (Bukhara, Republic of Uzbekistan). https://orcid.org/ 0000 0002 9178 3367
Teshaev Ulugbek ShukhratovichAssistant of the Department of Faculty and Hospital Surgery, PhD. Bukhara State Medical Institute named after Abu Ali ibn Sino. Bukhara, Uzbekistan https://orcid.org/0009-0000-0052-2827
Khidirov Ziyadulla ErkinovichHuman Anatomiya Assistant. Samarkand state medical University. Samarkand, Uzbekistan. https://orcid.org/0009-0000-2681-9610
Qodirov Oybek O‘ktam o‘g‘li Department of Gistology, Sitology Va Embryology, Bukhara State Medical Institute named after Abu Ali ibn Sino, Bukhara, Republic of Uzbekistan. https://orcid.org/0009-0000-1723-4303
Experimental renal failure is associated with systemic pathological alterations affecting the cardiovascular system. This study aimed to evaluate morphometric, histopathological, and immunohistochemical changes in the myocardium of rats with cisplatin-induced renal failure.
Morphometric analysis revealed progressive myocardial remodeling characterized by increased thickness of the endocardium, myocardium, and epicardium, as well as enlargement of cardiomyocytes and expansion of myocardial stromal tissue. Histopathological examination demonstrated vascular congestion, endothelial swelling, luminal narrowing, interstitial edema, inflammatory cell infiltration, and degenerative changes in cardiomyocytes.
Immunohistochemical analysis showed positive p53 expression in 37.75% of myocardial cells, indicating activation of apoptosis-related pathways. The severity of structural alterations increased with age and was accompanied by progressive vascular and stromal remodeling.
These findings demonstrate that cisplatin-induced renal failure causes significant myocardial injury through mechanisms involving microcirculatory disturbances, inflammation, and apoptosis, providing morphological evidence for the development of cardiorenal syndrome.