These double strand breaks are repaired by endogenous cellular repair pathways, primarily nonhomologous end joining (NHEJ) and homologous recombination (HR) [64, 98]
Conversely, if a patient presents with pernicious anemia or severe neurological signssuch as intense tingling in the hands, memory loss, or muscle weaknessthe dosage remains the same (usually 1,000 mcg), but the frequency increases significantly
Addressing these gaps requires multi-dimensional studies integrating single-cell omics, spatial transcriptomics, and clinical cohort analyses to resolve pathway crosstalk, define cell type-specific roles, and bridge preclinical and clinical translation, ultimately advancing ferroptosis-targeted strategies from bench to bedside in AKI treatment
Oxidative stress plays a vital role in these conditions