Cellular physiology as a basis for disease mechanisms and therapeutic targets
Keywords:
Cellular physiology, homeostasis, disease, signal transduction, oxidative stress, therapeutic targetsAbstract
Cellular physiology is a crucial framework for understanding the mechanisms that maintain normal biological function and underlie disease development at the cellular level. This review aimed to synthesize current knowledge on key cellular physiological processes, including homeostasis regulation, membrane transport, signal transduction, energy metabolism, and intercellular communication, and their role in disease pathogenesis when dysfunctional. This review, which focuses on the connection between compromised cellular physiology and human disease mechanisms, employs a narrative review methodology based on the most recent scientific literature from pertinent biomedical databases. The review shows that many major diseases, such as cancer, metabolic disorders, neurodegenerative diseases, and infectious diseases, are largely caused by dysfunction in fundamental cellular processes, such as mitochondrial disorders, oxidative stress imbalance, abnormal activation of signaling pathways, and impaired cellular communication. These events are linked in intricate regulatory networks that control cell responses and destiny rather than happening in isolation. Potential therapeutic targets, including signaling molecules, metabolic regulators, ion channels, and pathways leading to programmed cell death, have been identified thanks to developments in molecular biology and systems biology. This encourages a change in treatment techniques away from only treating clinical symptoms and toward mechanism-based tactics that concentrate on reestablishing cellular equilibrium. Precision medicine and tailored therapy are based on cellular physiology, which provides a vital connection between fundamental biological systems and therapeutic applications.
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Copyright (c) 2026 Journal of Advanced Veterinary Research

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license