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Tampe B, Tampe D, Zeisberg EM, et al. Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease. EBioMedicine. 2015;2(1):19-36doi: 10.1016/j.ebiom.2014.11.005.
Tampe, B., Tampe, D., Zeisberg, E. M., Müller, G. A., Bechtel-Walz, W., Koziolek, M., Kalluri, R., & Zeisberg, M. (2015). Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease. EBioMedicine, 2(1), 19-36. https://doi.org/10.1016/j.ebiom.2014.11.005
Tampe, Björn, et al. "Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease." EBioMedicine vol. 2,1 (2015): 19-36. doi: https://doi.org/10.1016/j.ebiom.2014.11.005
Tampe B, Tampe D, Zeisberg EM, Müller GA, Bechtel-Walz W, Koziolek M, Kalluri R, Zeisberg M. Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease. EBioMedicine. 2015 Jan;2(1):19-36. doi: 10.1016/j.ebiom.2014.11.005. PMID: 25717475; PMCID: PMC4337426.
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EBioMedicine. 2015 Jan;2(1):19-36. doi: 10.1016/j.ebiom.2014.11.005.

Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease.

EBioMedicine

Björn Tampe, Desiree Tampe, Elisabeth M Zeisberg, Gerhard A Müller, Wibke Bechtel-Walz, Michael Koziolek, Raghu Kalluri, Michael Zeisberg

Affiliations

  1. Department of Nephrology and Rheumatology, Göttingen University Medical Center, Georg August University, Robert Koch Street 40, Göttingen, Germany ; Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA, USA.
  2. Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA, USA ; Department of Cardiology and Pneumology, Göttingen University Medical Center, Georg August University, Robert Koch Street 40, Göttingen, Germany ; German Center for Cardiovascular Research (DZHK), Robert Koch Street 40, Göttingen, Germany.
  3. Department of Nephrology and Rheumatology, Göttingen University Medical Center, Georg August University, Robert Koch Street 40, Göttingen, Germany.
  4. Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA, USA ; Renal Division, University Hospital Freiburg, Hugstetter Street 55, Freiburg, Germany.
  5. Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA, USA ; Department of Cancer Biology and the Metastasis Research Center, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX, USA.

PMID: 25717475 PMCID: PMC4337426 DOI: 10.1016/j.ebiom.2014.11.005

Abstract

Progression of chronic kidney disease remains a principal problem in clinical nephrology and there is a pressing need for novel therapeutics and biomarkers. Aberrant promoter CpG island methylation and subsequent transcriptional silencing of specific genes have emerged as contributors to progression of chronic kidney disease. Here, we report that transcriptional silencing of the Ras-GTP suppressor RASAL1 contributes causally to progression of kidney fibrosis and we identified that circulating methylated

Keywords: DNA methylation; De-methylation; Epigenetics; Fibrosis; RASAL1; Ten-Eleven Translocation (TET)

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