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Systemically administered tempol reduces neuronal activity in paraventricular nucleus of hypothalamus and rostral ventrolateral medulla in ratsSymbolic analysis detects alterations of cardiac autonomic modulation in congestive heart failure ratsCentral SDF-1/CXCL12 expression and its cardiovascular and sympathetic effects: the role of angiotensin II, TNF-α, and MAP kinase signaling.Proinflammatory cytokines upregulate sympathoexcitatory mechanisms in the subfornical organ of the rat.Peroxisome proliferator-activated receptor-γ regulates inflammation and renin-angiotensin system activity in the hypothalamic paraventricular nucleus and ameliorates peripheral manifestations of heart failure.Activation of central PPAR-γ attenuates angiotensin II-induced hypertension.Aldosterone-induced brain MAPK signaling and sympathetic excitation are angiotensin II type-1 receptor dependentCentral actions of the chemokine stromal cell-derived factor 1 contribute to neurohumoral excitation in heart failure ratsInhibition of Brain Mitogen-Activated Protein Kinase Signaling Reduces Central Endoplasmic Reticulum Stress and Inflammation and Sympathetic Nerve Activity in Heart Failure Rats.ERK1/2 MAPK signaling in hypothalamic paraventricular nucleus contributes to sympathetic excitation in rats with heart failure after myocardial infarction.Subfornical organ mediates sympathetic and hemodynamic responses to blood-borne proinflammatory cytokines.Angiotensin II upregulates hypothalamic AT1 receptor expression in rats via the mitogen-activated protein kinase pathway.Angiotensin II-triggered p44/42 mitogen-activated protein kinase mediates sympathetic excitation in heart failure rats.Does aldosterone upregulate the brain renin-angiotensin system in rats with heart failure?Endoplasmic reticulum stress increases brain MAPK signaling, inflammation and renin-angiotensin system activity and sympathetic nerve activity in heart failure.Brain perivascular macrophages and the sympathetic response to inflammation in rats after myocardial infarction.Autonomic cardiovascular modulation.Brain angiotensin-converting enzyme activity and autonomic regulation in heart failure.TNF-α receptor 1 knockdown in the subfornical organ ameliorates sympathetic excitation and cardiac hemodynamics in heart failure rats.Increased cyclooxygenase-2 expression in hypothalamic paraventricular nucleus in rats with heart failure: role of nuclear factor kappaB.11beta-hydroxysteroid dehydrogenase type 2 activity in hypothalamic paraventricular nucleus modulates sympathetic excitation.Angiotensin II Type 1a Receptors in the Subfornical Organ Modulate Neuroinflammation in the Hypothalamic Paraventricular Nucleus in Heart Failure Rats.
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description
researcher ORCID ID = 0000-0003-4404-4059
@en
wetenschapper
@nl
name
Shun-Guang Wei
@ast
Shun-Guang Wei
@en
Shun-Guang Wei
@es
Shun-Guang Wei
@nl
type
label
Shun-Guang Wei
@ast
Shun-Guang Wei
@en
Shun-Guang Wei
@es
Shun-Guang Wei
@nl
prefLabel
Shun-Guang Wei
@ast
Shun-Guang Wei
@en
Shun-Guang Wei
@es
Shun-Guang Wei
@nl
P106
P1153
7401765309
P31
P496
0000-0003-4404-4059