Human papillomavirus (HPV)-positive cervical cancer develops under persistent metabolic, replicative, and oxidative stress and frequently exhibits limited sensitivity or acquired resistance to cisplatin-based concurrent chemoradiotherapy (CCRT). In this context, ferroptosis represents a potential therapeutic vulnerability, yet the regulatory networks that sustain ferroptosis resistance in HPV-positive tumors remain incompletely defined. This review proposes a mitochondria-centered framework in which mitochondrial STAT3 (mitoSTAT3), electron transport chain (ETC)-dependent coenzyme Q (CoQ) redox turnover, and dihydroorotate dehydrogenase (DHODH) may form a context-dependent regulatory axis of ferroptosis defense. We first summarize how HPV E6 and E7 oncoproteins impose chronic biosynthetic, replicative, and oxidative pressures that increase tumor dependence on mitochondrial redox and bioenergetic control. We then discuss STAT3 not only as a canonical nuclear transcription factor but also as a stress-adaptive signaling node with mitochondria-associated functions. Current evidence suggests that mitoSTAT3 may support ETC efficiency, limit electron leakage, and help maintain CoQ cycling, whereas DHODH may contribute to localized CoQH2-dependent radical-trapping activity within the inner mitochondrial membrane. Together, these mechanisms may restrain mitochondrial lipid peroxidation and thereby reduce susceptibility to ferroptotic injury. Finally, we discuss the translational implications of this framework, including ferroptosis-sensitizing strategies, DHODH inhibition, STAT3-directed interventions, biomarker-guided patient stratification, rational combinations with chemoradiotherapy or immunotherapy, and nanomedicine-enabled delivery. Overall, this review identifies the mitoSTAT3-DHODH axis as a mechanistically plausible regulatory network of ferroptosis resistance and a potential therapeutic vulnerability in HPV-positive cervical cancer.