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This narrative review synthesizes current evidence on pterostilbene in oxidative stress-related diseases, focusing on its chemical and pharmacokinetic basis, redox-related signaling responses, disease-specific evidence, and translational challenges. Most available evidence comes from preclinical models and suggests that the biological effects of pterostilbene cannot be explained solely by direct reactive oxygen species (ROS) scavenging. Instead, pterostilbene is associated with several redox-sensitive processes, including Nrf2-related antioxidant responses, redox-inflammatory crosstalk, mitochondria-associated stress responses, metabolic regulation, and cell death-related pathways. Evidence from osteoarthritis, neurodegenerative and cognitive dysfunction models, ischemia-reperfusion injury, metabolic diseases, and cancer indicates that these effects vary substantially across pathological contexts. In non-malignant degenerative, ischemic, and metabolic models, pterostilbene is generally associated with attenuation of oxidative stress-, inflammation-, or cellular stress-related injury markers, whereas in selected cancer models it may disrupt redox-adapted tumor-cell stress tolerance and promote apoptosis- or pyroptosis-related responses. Important translational barriers remain, including incomplete direct target validation, heterogeneous dosing and intervention designs, reliance on static oxidative stress endpoints, limited clinical validation, and insufficient integration of negative or context-dependent findings. By applying a redox homeostasis-centered framework, this review clarifies the contexts in which pterostilbene effects have been reported and identifies the evidence needed before disease-specific translational positioning can be established.