Khalid Nayab, Akram Zertashia, Hayat Nighat, Siddique Ambar, Gul Asma, Wajid Hifza
Cancer Genetics and Epigenetics Lab, Department of Biosciences, COMSATS University Islamabad, Islamabad, Pakistan.
Department of Biosciences, Islamic International University Islamabad, Islamabad, Pakistan.
Biochem Genet. 2025 Jul 18. doi: 10.1007/s10528-025-11188-y.
Acute kidney disease (AKD), a condition between AKI and CKD, was categorized as a separate entity by KDIGO in 2012, although it remains debatable. The present study investigates mechanism underlying AKD condition with ferroptosis, lipid peroxidation and related genes. Blood samples were collected from AKD patients (n = 100) along with age and gender matched control. Expression analysis of GPX4, EPO, TF, HP, FTH1, NCOA4 genes was done using RT-PCR. Peroxidase activity, lipid peroxidation, serum ferritin and total protein were measured. Relative expressions of GPX4, EPO and TF were downregulated (P < 0.001) while FTH1, HP and NCOA4 expression were upregulated (P < 0.001) in AKD group compared to controls. Similar trend was observed between male AKD group versus male control (P < 0.001) and female AKD group versus female controls (P < 0.001). Expression deregulation of selected genes was detected in both age groups (≤ 40 year & > 40 year age) of AKD patents compared to their respective controls. AKD group showed significant (P < 0.001) increase in serum ferritin levels compared to respective control. Low activity of POD and elevated levels of lipid peroxidation was observed in male (P < 0.001) and female (P < 0.01) AKD patients compared to controls. Present study suggested a positive contribution of lipid-mediated ferroptosis in progression of AKD. Furthermore, expression deregulation of genes underlying iron metabolism along with depleted expression of antioxidant gene and low peroxidase activity postulated iron overload as possible candidate in etiology of AKD condition.
急性肾脏病(AKD)是介于急性肾损伤(AKI)和慢性肾脏病(CKD)之间的一种病症,2012年被改善全球肾脏病预后组织(KDIGO)归类为一个独立的实体,尽管这一分类仍存在争议。本研究探讨了铁死亡、脂质过氧化及相关基因在AKD发病机制中的作用。收集了100例AKD患者以及年龄和性别相匹配的对照者的血样。采用逆转录聚合酶链反应(RT-PCR)检测谷胱甘肽过氧化物酶4(GPX4)、促红细胞生成素(EPO)、转铁蛋白(TF)、触珠蛋白(HP)、铁蛋白重链1(FTH1)、核受体辅激活因子4(NCOA4)基因的表达。检测过氧化物酶活性、脂质过氧化、血清铁蛋白和总蛋白水平。与对照组相比,AKD组中GPX4、EPO和TF的相对表达下调(P<0.001),而FTH1、HP和NCOA4的表达上调(P<0.001)。男性AKD组与男性对照组(P<0.001)以及女性AKD组与女性对照组(P<0.001)之间也观察到类似趋势。与各自的对照组相比,在AKD患者的两个年龄组(≤40岁和>40岁)中均检测到所选基因的表达失调。与各自的对照组相比,AKD组的血清铁蛋白水平显著升高(P<0.001)。与对照组相比,男性(P<0.001)和女性(P<0.01)AKD患者的过氧化物酶活性较低,脂质过氧化水平升高。本研究表明脂质介导的铁死亡在AKD进展中起积极作用。此外,铁代谢相关基因的表达失调、抗氧化基因表达减少以及过氧化物酶活性降低表明铁过载可能是AKD发病机制中的候选因素。