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Low adenosine triphosphate (ATP) is a major cause of ischemic white matter injury. ATP depletion deprives axons and oligodendrocytes of the energy needed to maintain ionic gradients, leading to ion pump failure, calcium toxicity, demyelination, and ultimately cell death. Mechanisms of Injury Na⁺/K⁺-ATPase failure: ATP depletion disables sodium-potassium pumps, causing sodium and water to accumulate inside axons, resulting in cytotoxic swelling. Calcium overload: Excess intracellular calcium activates destructive enzymes (calpains and phospholipases) that degrade the cytoskeleton and cell membranes. Oligodendrocyte loss: Oligodendrocytes, which produce and maintain myelin, are highly energy-dependent. ATP depletion triggers apoptosis, leading to demyelination and impaired axonal conduction. Why White Matter Is Highly Vulnerable White matter is particularly susceptible to ischemia because it: Has a relatively sparse collateral blood supply. Lies within watershed regions that are vuln...

Revision:  Abstract Mitochondria generate ATP while regulating calcium signaling, apoptosis, metabolism, immune responses, and reactive oxygen species (ROS). Because organs with high energy demands—including the brain, heart, skeletal muscle, retina, cochlea, liver, endocrine glands, and immune system—depend heavily on mitochondrial function, mitochondrial dysfunction contributes to aging and diseases affecting multiple organ systems. This review summarizes the roles of mitochondria in neurodegeneration, immunity, circulation, endocrine physiology, muscle and skin homeostasis, vision, hearing, mitochondrial genetics, and emerging therapeutic strategies. Introduction Mitochondria evolved from an ancestral bacterium through endosymbiosis approximately two billion years ago and remain indispensable for eukaryotic life. In addition to ATP production, they regulate calcium homeostasis, apoptosis, redox balance, innate immunity, and metabolic adaptation. Although mitochondria possess the...