Ghajar-Rahimi Gelare, Traylor Amie M, Mathew Bini, Bostwick James R, Nebane N Miranda, Zmijewska Anna A, Esman Stephanie K, Thukral Saakshi, Zhai Ling, Sambandam Vijaya, Cowell Rita M, Suto Mark J, George James F, Augelli-Szafran Corinne E, Agarwal Anupam
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Antioxidants (Basel). 2022 Sep 23;11(10):1888. doi: 10.3390/antiox11101888.
Acute kidney injury (AKI) is a major public health concern with significant morbidity and mortality and no current treatments beyond supportive care and dialysis. Preclinical studies have suggested that heme-oxygenase-1 (HO-1), an enzyme that catalyzes the breakdown of heme, has promise as a potential therapeutic target for AKI. Clinical trials involving HO-1 products (biliverdin, carbon monoxide, and iron), however, have not progressed beyond the Phase ½ level. We identified small-molecule inducers of HO-1 that enable us to exploit the full therapeutic potential of HO-1, the combination of its products, and yet-undefined effects of the enzyme system. Through cell-based, high-throughput screens for induction of HO-1 driven by the human HO-1 promoter/enhancer, we identified two novel small molecules and broxaldine (an FDA-approved drug) for further consideration as candidate compounds exhibiting an Emax ≥70% of 5 µM hemin and EC50 <10 µM. RNA sequencing identified shared binding motifs to NRF2, a transcription factor known to regulate antioxidant genes, including HMOX1. In vitro, the cytoprotective function of the candidates was assessed against cisplatin-induced cytotoxicity and apoptosis. In vivo, delivery of a candidate compound induced HO-1 expression in the kidneys of mice. This study serves as the basis for further development of small-molecule HO-1 inducers as preventative or therapeutic interventions for a variety of pathologies, including AKI.
急性肾损伤(AKI)是一个重大的公共卫生问题,具有较高的发病率和死亡率,目前除了支持治疗和透析外没有其他治疗方法。临床前研究表明,血红素加氧酶-1(HO-1)是一种催化血红素分解的酶,有望成为AKI的潜在治疗靶点。然而,涉及HO-1产物(胆红素、一氧化碳和铁)的临床试验尚未超过1/2期水平。我们鉴定出了HO-1的小分子诱导剂,使我们能够充分利用HO-1的治疗潜力、其产物的组合以及该酶系统尚未明确的作用。通过基于细胞的、由人HO-1启动子/增强子驱动的HO-1诱导的高通量筛选,我们鉴定出了两种新型小分子和溴沙定(一种FDA批准的药物),作为候选化合物进一步考虑,其表现出Emax≥5μM血红素的70%且EC50<10μM。RNA测序确定了与NRF2的共同结合基序,NRF2是一种已知调节抗氧化基因(包括HMOX1)的转录因子。在体外,评估了候选物对顺铂诱导的细胞毒性和凋亡的细胞保护功能。在体内,一种候选化合物的给药诱导了小鼠肾脏中HO-1的表达。这项研究为进一步开发小分子HO-1诱导剂作为包括AKI在内的多种病理的预防或治疗干预措施奠定了基础。