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2017 ; 5
(9
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Early activation of deleterious molecular pathways in the kidney in experimental
heart failure with atrial remodeling
#MMPMID28507167
Ichiki T
; Huntley BK
; Harty GJ
; Sangaralingham SJ
; Burnett JC Jr
Physiol Rep
2017[May]; 5
(9
): ä PMID28507167
show ga
Heart failure (HF) is a major health problem with worsening outcomes when renal
impairment is present. Therapeutics for early phase HF may be effective for
cardiorenal protection, however the detailed characteristics of the kidney in
early-stage HF (ES-HF), and therefore treatment for potential renal protection,
are poorly defined. We sought to determine the gene and protein expression
profiles of specific maladaptive pathways of ES-HF in the kidney and heart.
Experimental canine ES-HF, characterized by de-novo HF with atrial remodeling but
not ventricular fibrosis, was induced by right ventricular pacing for 10 days.
Kidney cortex (KC), medulla (KM), left ventricle (LV), and left atrial (LA)
tissues from ES-HF versus normal canines (n = 4 of each) were analyzed using
RT-PCR microarrays and protein assays to assess genes and proteins related to
inflammation, renal injury, apoptosis, and fibrosis. ES-HF was characterized by
increased circulating natriuretic peptides and components of the
renin-angiotensin-aldosterone system and decreased sodium and water excretion
with mild renal injury and up-regulation of CNP and renin genes in the kidney.
Compared to normals, widespread genes, especially genes of the inflammatory
pathways, were up-regulated in KC similar to increases seen in LA Protein
expressions related to inflammatory cytokines were also augmented in the KC Gene
and protein changes were less prominent in the LV and KM The ES-HF displayed mild
renal injury with widespread gene changes and increased inflammatory cytokines.
These changes may provide important clues into the pathophysiology of ES-HF and
for therapeutic molecular targets in the kidney of ES-HF.
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