Genetic disruption of Npr1 depletes regulatory T cells and provokes high levels of proinflammatory cytokines and fibrosis in the kidneys of female mutant mice

Lignende værker

• Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice
  af: Subramanian, Umadevi, et al.
  Udgivet: (2016)
• Targeted Disruption of Guanylyl Cyclase-A/Natriuretic Peptide Receptor-A Gene Provokes Renal Fibrosis and Remodeling in Null Mutant Mice: Role of Proinflammatory Cytokines
  af: Das, Subhankar, et al.
  Udgivet: (2010)
• Inhibition of HDAC enhances STAT acetylation, blocks NF-κB, and suppresses the renal inflammation and fibrosis in Npr1 haplotype male mice
  af: Kumar, Prerna, et al.
  Udgivet: (2017)
• Genetically Altered Mutant Mouse Models of Guanylyl Cyclase/Natriuretic Peptide Receptor-A Exhibit the Cardiac Expression of Proinflammatory Mediators in a Gene-Dose-Dependent Manner
  af: Vellaichamy, Elangovan, et al.
  Udgivet: (2014)
• Genetic disruption of guanylyl cyclase/natriuretic peptide receptor-A upregulates renal (pro)renin receptor expression in Npr1 null mutant mice
  af: Periyasamy, Ramu, et al.
  Udgivet: (2019)