Zhang Yize, Arzaghi Hamidreza, Ma Zhehan, Roye Yasmin, Musah Samira
Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA.
Center for Biomolecular and Tissue Engineering, Duke University, Durham, NC 27708, USA.
Biomedicines. 2024 Nov 16;12(11):2622. doi: 10.3390/biomedicines12112622.
Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD), contributing to significant morbidity, mortality, and rising healthcare costs. In this review article, we explore the role of epigenetic mechanisms in HN progression and their potential therapeutic implications. We begin by examining key epigenetic modifications-DNA methylation, histone modifications, and non-coding RNAs-observed in kidney disease. Next, we discuss the underlying pathophysiology of HN and highlight current in vitro and in vivo models used to study the condition. Finally, we compare various types of HN-induced renal injury and their associated epigenetic mechanisms with those observed in other kidney injury models, drawing inferences on potential epigenetic therapies for HN. The information gathered in this work indicate that epigenetic mechanisms can drive the progression of HN by regulating key molecular signaling pathways involved in renal damage and fibrosis. The limitations of Renin-Angiotensin-Aldosterone System (RAAS) inhibitors underscore the need for alternative treatments targeting epigenetic pathways. This review emphasizes the importance of further research into the epigenetic regulation of HN to develop more effective therapies and preventive strategies. Identifying novel epigenetic markers could provide new therapeutic opportunities for managing CKD and reducing the burden of ESRD.
高血压肾病（HN）是慢性肾脏病（CKD）和终末期肾病（ESRD）的主要病因，导致了显著的发病率、死亡率以及不断上升的医疗成本。在这篇综述文章中，我们探讨了表观遗传机制在高血压肾病进展中的作用及其潜在的治疗意义。我们首先研究在肾脏疾病中观察到的关键表观遗传修饰——DNA甲基化、组蛋白修饰和非编码RNA。接下来，我们讨论高血压肾病的潜在病理生理学，并重点介绍目前用于研究该病症的体外和体内模型。最后，我们将各种类型的高血压肾病诱导的肾损伤及其相关的表观遗传机制与在其他肾损伤模型中观察到的进行比较，推断出针对高血压肾病的潜在表观遗传治疗方法。这项工作收集的信息表明，表观遗传机制可通过调节参与肾损伤和纤维化的关键分子信号通路来推动高血压肾病的进展。肾素 - 血管紧张素 - 醛固酮系统（RAAS）抑制剂的局限性凸显了针对表观遗传途径的替代治疗的必要性。这篇综述强调了进一步研究高血压肾病的表观遗传调控以开发更有效治疗方法和预防策略的重要性。识别新的表观遗传标志物可为管理慢性肾脏病和减轻终末期肾病负担提供新的治疗机会。
