http://researchonline.federation.edu.au/vital/access/manager/Index en-us 5 http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13342 Wed 07 Apr 2021 14:01:30 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10534 Wed 07 Apr 2021 13:55:52 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17466 1000 common and rare genetic variants associated with BP and/or hypertension. The kidney is not only an organ of key relevance to BP regulation and the development of hypertension, but it also acts as the tissue mediator of genetic predisposition to hypertension. The identity of kidney genes, pathways, and related mechanisms underlying the genetic associations with BP has started to emerge through integration of genomics with kidney transcriptomics, epigenomics, and other omics as well as through applications of causal inference, such as Mendelian randomization. Single-cell methods further enabled mapping of BP-associated kidney genes to cell types, and in conjunction with other omics, started to illuminate the biological mechanisms underpinning associations of BP-associated genetic variants and kidney genes. Polygenic risk scores derived from genome-wide association studies and refined on kidney omics hold the promise of enhanced diagnostic prediction, whereas kidney omics-informed drug discovery is likely to contribute new therapeutic opportunities for hypertension and hypertension-mediated kidney damage. © 2022 International Society of Nephrology]]> Thu 23 Mar 2023 11:55:08 AEDT ]]>