ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO763

Revealing Novel Signaling Pathways Affected in Glomeruli During Salt-Sensitive Hypertension

Session Information

  • Hypertension and CVD: Mechanisms
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

  • 1503 Hypertension and CVD: Mechanisms


  • Anwar, Fabiha, Augusta University, Augusta, Georgia, United States
  • Lysikova, Daria, Augusta University, Augusta, Georgia, United States
  • Schibalski, Ryan, Augusta University, Augusta, Georgia, United States
  • Domondon, Mark, Medical University of South Carolina, Charleston, South Carolina, United States
  • Shamatova, Margarita, Augusta University, Augusta, Georgia, United States
  • Stadler, Krisztian, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States
  • Spires, Denisha R., Augusta University, Augusta, Georgia, United States
  • Ilatovskaya, Daria, Augusta University, Augusta, Georgia, United States

Salt-sensitive hypertension (SS-HTN) is defined by an increase in blood pressure resulting from an elevated salt intake; it is characterized by the development of hypertensive glomerulosclerosis. There is a gap in knowledge regarding factors that might contribute to glomerular damage in SS-HTN. The goal of this study was to assess the transcriptomic changes that accompany glomerulosclerosis in SS-HTN.


8-week-old Dahl Salt Sensitive rats were fed a normal (0.4% NaCl, NS) or high salt diet (4% NaCl, HS, to induce hypertension) for 3 weeks. At the endpoint, glomeruli were obtained from the cortex using differential sieving. Total mRNA was isolated from the glomeruli and subjected to NextGen sequencing; transcriptomic data was analyzed using IPA software. The cutoff value for the experimental fold-change (EFC) was 1.5; p value < 0.05 was considered significant.


149 genes were found to be differentially expressed in glomeruli from HS and NS diet fed rats (107 and 42 were down- and up-regulated). We recorded changes in several signaling pathways: GPCR signaling was suppressed, including leptin/melanocortin, AMPK/mTOR, and ERK/MAPK pathways (Elf3 (EFC 1.8); Mc4r (-5.0), Gator2 (-4.3), Azgp1 (-3.6), Lepr (-2.9), Nr4a1 (-2.4), Pki (-2.5), Rgs2 (-1.8)). We report changes in calcium regulation (Calb (1.6), Cav2.1 (-3.6), Prkce (-3.0), Carf (-2.2), Ip3kb (-1.8)), cellular metabolism (Ltc4s (2.3), Apobec1 (1.5), Sdr42e1 (1.5), Acaca (-3.2), Fads3 (-2.6), Sdhaf3 (-2.3), Ren (-1.9), Cox14 (-1.7), Cyp4f2 (-1.6), Mgll (-1.6) Cyp2d22 (-1.5), Ch25h (-1.5), Gnpda2 (-1.5)), immune response, apoptosis, and inflammation (Mrc1 (1.5), NFkB (-2.8), Xiap (-2.8), Fcgr2a (-2.7), Marco (-2), Hla-a (-1.7)), as well as fibrosis and cell proliferation (Myl3 (1.7), Ccnd2 (1.5), Fmnl3 (-3.5), c-Rel (-2.8), Cdk13 (-1.8), Cdkn1b (-1.6), Wnt5a (-1.6)), and solute transporters (Slc14a1 (2.8), Slco1a1 (-2.2), Slc2a10 (-1.7), Slc38a3 (-1.7), Slc6a6 (-1.6), Slc38a6 (-1.5)).


We revealed here novel gene networks affected in glomeruli during SS-HTN. Alignment of this data with other existing ‘omics analyses is necessary to provide further insight into the development of hypertensive glomerulosclerosis.


  • Other NIH Support