Elizaveta I. Bon1*, Maksimovich Nataliya Yevgenyevna1, Dremza Iosif Karlovich1, Zorko AI1
1Grodno State Medical University, Gorkogo St, Grodno, Republic of Belarus
*Corresponding author: Elizaveta I Bon, Candidate of Biological Science, Assistant Professor of Pathophysiology Department named D. A. Maslakov, Grodno State Medical University, Grodno State Medical University, 80 Gorky St,230009, Grodno, Belarus, Phone: 80336878764, E-mail: [email protected]
Received : May 28, 2025
Published : June 26, 2026
Citation: Bon EI, et al. (2026). Cellular Pathology: Fundamental Mechanisms of Damage, Dysfunction, and Death. Gastro Res. 5(1):15.
Copyright: Bon EI, et al. © (2026).
ABSTRACT
The cell constitutes the fundamental structural and functional unit of all tissues and organs in multicellular organisms. As a self-regulating biological system, it integrates a vast array of specific, metabolic, energetic, protective, and informational functions.
Cellular pathology, characterized by structural and functional disturbances, represents the foundational pathological process underlying human disease. This article provides a comprehensive overview of the core principles of cell damage, detailing the principal mechanisms of injury, including energy metabolism disruption, membrane and enzyme system damage, ion imbalance, genetic program dysregulation, and signaling pathway failures. The molecular pathways and morphological features of the main types of cell death—necrosis, apoptosis, autophagy, and senescence—are examined. Furthermore, the review explores the critical role of mitochondrial and lysosomal pathology, outlines fundamental cellular adaptation mechanisms, and discusses specific disease entities arising from organelle dysfunction, such as lysosomal storage disorders. Understanding these processes is essential for deciphering the pathogenesis of a wide spectrum of conditions, from ischemic injury and neurodegenerative diseases to cancer and inherited metabolic disorders.
Keywords: Cell Pathology, Oxidative Stress, Apoptosis, Necrosis, Mitochondrial Dysfunction, Reactive Oxygen Species (ROS), Lysosomal Storage Diseases, Signal Transduction, Autophagy, Cellular Adaptation