| Autor: |
Zhang Y; Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA., Arzaghi H; Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA., Ma Z; Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA., Roye Y; Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA., Musah S; 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.; Division of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.; Department of Cell Biology, Duke University, Durham, NC 27710, USA.; Affiliate Faculty of the Developmental and Stem Cell Biology Program, Duke Regeneration Center, and Duke MEDx Initiative, Duke University, Durham, NC 27710, USA. |
| Abstrakt: |
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. |
