Nickan Research Institute Journal of Renal Injury Prevention 2345-2781 15 3 2026 09 01 Mechanisms of endothelial dysfunction and tubulointerstitial fibrosis in radiation-induced kidney injury e38761 e38761 10.34172/jrip.38761 EN Maktuba Mirrakhimova https://orcid.org/0000-0003-2802-4357 Qaxramon О’rinboyev https://orcid.org/0009-0009-2895-212X Jurabek Saloxiddinov https://orcid.org/0009-0003-6562-0112 Ravshan Makhmudov https://orcid.org/0009-0008-8394-6323 Umidjon Islamov https://orcid.org/0009-0004-3678-1950 Jasur Saidov https://orcid.org/0009-0007-1601-1838 Doniyorbek Khasanov https://orcid.org/0000-0003-3911-7321 Aziza Mirzaraximova https://orcid.org/0009-0009-1077-4599 Akramjon Teshaboyev https://orcid.org/0009-0001-6850-4489 Muhtorali Umarkulov https://orcid.org/0009-0000-9942-234X Journal Article 10.34172/jrip.38761 2026 03 27 2026 05 18 Radiation-induced kidney injury embodies a convergent process in which endothelial dysfunction initiates and perpetuates tubulointerstitial fibrosis through oxidative stress, inflammatory cell recruitment, microvascular collapse, and disturbed cellular plasticity. The sequence begins with endothelial apoptosis and barrier breakdown, evolves through chronic hypoxia and fibrosis-promoting signaling, and culminates in irreversible architectural remodeling that compromises renal filtration and oxygen delivery. The hallmark mechanisms include reactive oxygen species-mediated eNOS uncoupling, sustained nuclear factor-kappa B (NF-κB) and transforming growth factor-beta (TGF-β) activation, endothelial-to-mesenchymal (EndMT) and epithelial-to-mesenchymal (EMT) transitions, microvascular rarefaction, and senescent secretory phenotypes – all contributing to a feed-forward loop that defines radiation nephropathy as a progressive, self-amplifying vascular-fibrotic syndrome.