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РецензированоEN2025

MOLECULAR AND FUNCTIONAL MECHANISMS OF CARDIAC PATHOPHYSIOLOGY: FROM CELLULAR INJURY TO ORGAN DYSFUNCTION

Хамидулло Ракхимов

Международный журнал искусственного интеллекта · 05 · 2025

Аннотация

Background: Cardiac pathophysiology is driven by a complex interaction of molecular, structural, and systemic factors that impair myocardial performance. Objective: To investigate the fundamental cellular and functional mechanisms contributing to cardiac dysfunction with a focus on ischemia-reperfusion injury, maladaptive remodeling, and electrophysiological disturbances. Methods: A narrative review and analytical synthesis of 2012–2024 experimental and clinical studies from PubMed and Scopus databases. The study evaluated alterations in myocardial energy metabolism, calcium signaling, and extracellular matrixremodeling. Results: Ischemia triggers ATP depletion and mitochondrial dysfunction, while reperfusion generates reactive oxygen species leading to oxidative damage. Persistent neurohormonal activation induces pathological hypertrophy and fibrosis, reducing ventricular compliance. Abnormal calcium cycling and gap junctionremodeling createarrhythmogenic substrates. Conclusion: Cardiac pathophysiology represents a dynamic continuum beginning at the molecular level and progressing to overt heart failure. Early detection of mitochondrial and calcium-handling abnormalities may providenovel therapeutic targets. Keywords: cardiac pathophysiology, ischemia-reperfusion injury, ventricular remodeling, mitochondrial dysfunction, calcium signaling, heart failure.

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«Background: Cardiac pathophysiology is driven by a complex interaction of molecular, structural, and systemic factors that impair myocardial performance.»

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Background: Cardiac pathophysiology is driven by a complex interaction of molecular, structural, and systemic factors that impair myocardial performance. Полный текст публикации CiteX не хранит — доступ к первоисточнику открывается по DOI согласно лицензии издателя и выбранному плану.

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cardiac pathophysiology, ischemia-reperfusion injury, ventricular remodeling
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