Congestive heart failure with reduced EF: Difference between revisions
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* It has been proposed that dysregulation in epigenetic signals, cellular messengers and molecular targets precedes pathological cardiac remodeling, disrupts progenitor cell functions, adversely affects the endogenous repair system, and metabolic pathways. | * It has been proposed that dysregulation in epigenetic signals, cellular messengers and molecular targets precedes pathological cardiac remodeling, disrupts progenitor cell functions, adversely affects the endogenous repair system, and metabolic pathways. | ||
*Hypoxia-inducible factor 1 (HIF-1) has been shown to be upregulated in HFrEF. This trasnscription activator is involved in various oxidation-reduction reactions, angiogenesis and vascular remodelling. Myocardial hypoxia leads to its activation which downstream produces elevated levels of brain natriuretic peptide (BNP). Hypoperfusion of peripheral organs leading to hypoxia is the key trigger for induction of increased HIF-1 activity.<ref name="pmid19542490">{{cite journal |vauthors=Casals G, Ros J, Sionis A, Davidson MM, Morales-Ruiz M, Jiménez W |title=Hypoxia induces B-type natriuretic peptide release in cell lines derived from human cardiomyocytes |journal=Am. J. Physiol. Heart Circ. Physiol. |volume=297 |issue=2 |pages=H550–5 |date=August 2009 |pmid=19542490 |doi=10.1152/ajpheart.00250.2009 |url=}}</ref> | *Hypoxia-inducible factor 1 (HIF-1) has been shown to be upregulated in HFrEF. This trasnscription activator is involved in various oxidation-reduction reactions, angiogenesis and vascular remodelling. Myocardial hypoxia leads to its activation which downstream produces elevated levels of brain natriuretic peptide (BNP). Hypoperfusion of peripheral organs leading to hypoxia is the key trigger for induction of increased HIF-1 activity.<ref name="pmid19542490">{{cite journal |vauthors=Casals G, Ros J, Sionis A, Davidson MM, Morales-Ruiz M, Jiménez W |title=Hypoxia induces B-type natriuretic peptide release in cell lines derived from human cardiomyocytes |journal=Am. J. Physiol. Heart Circ. Physiol. |volume=297 |issue=2 |pages=H550–5 |date=August 2009 |pmid=19542490 |doi=10.1152/ajpheart.00250.2009 |url=}}</ref><ref name="pmid19542490">{{cite journal |vauthors=Casals G, Ros J, Sionis A, Davidson MM, Morales-Ruiz M, Jiménez W |title=Hypoxia induces B-type natriuretic peptide release in cell lines derived from human cardiomyocytes |journal=Am. J. Physiol. Heart Circ. Physiol. |volume=297 |issue=2 |pages=H550–5 |date=August 2009 |pmid=19542490 |doi=10.1152/ajpheart.00250.2009 |url=}}</ref> | ||
=== Protein kinase B signalling === | === Protein kinase B signalling === | ||
Revision as of 20:31, 23 December 2019
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Heart Failure With Reduced Ejection Fraction (HFrEF)
The pathogenesis of HFrEF is related largely to cellular proliferation and metabolism
Activation of DNA binding transcription factors
- It has been proposed that dysregulation in epigenetic signals, cellular messengers and molecular targets precedes pathological cardiac remodeling, disrupts progenitor cell functions, adversely affects the endogenous repair system, and metabolic pathways.
- Hypoxia-inducible factor 1 (HIF-1) has been shown to be upregulated in HFrEF. This trasnscription activator is involved in various oxidation-reduction reactions, angiogenesis and vascular remodelling. Myocardial hypoxia leads to its activation which downstream produces elevated levels of brain natriuretic peptide (BNP). Hypoperfusion of peripheral organs leading to hypoxia is the key trigger for induction of increased HIF-1 activity.[1][1]
Protein kinase B signalling
MAPK cascade
Dysregulation of cellular protein metabolic pathways
Role of ERK1 and ERK2 pathways
Role of nitric oxide biosynthetic pathway
Smooth muscle cell proliferation
ATF2 mediated hypertrophy
Major biomarkers of HFrEF
NT-proBNP, GDF-15, and IL1RL1