ArticleHypertension (Dallas, Tex. : 1979)2016
Inhibition of Brain Mitogen-Activated Protein Kinase Signaling Reduces Central Endoplasmic Reticulum Stress and Inflammation and Sympathetic Nerve Activity in Heart Failure Rats.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Networked Pathological Mechanisms of Central Sympathetic Nervous System Regulation in Heart Failure and Novel Paradigms for Targeted Intervention.International journal of molecular sciences · 2026Review
- Role of Sigma-1 Receptors in the Paraventricular Nucleus and Myocardium during Cirrhotic Cardiomyopathy in Rats.Molecular neurobiology · 2026Article
- The heart-brain crosstalk in age related cardiovascular and neurodegenerative diseases.Fluids and barriers of the CNS · 2025Review
- Uncovering the molecular mechanisms of tonifying kidney and activating blood Decoction against myocardial fibrosis using network Pharmacology and experimental validation.Scientific reports · 2025Article
- Neuro-immune interactions in coronary microvascular disease: mechanisms and therapeutic prospect.Frontiers in immunology · 2025Review
- Article
- EETs/sEHi alleviates nociception by blocking the crosslink between endoplasmic reticulum stress and neuroinflammation in a central poststroke pain model.Journal of neuroinflammation · 2021Article
- Article
- An injectable microparticle formulation for the sustained release of the specific MEK inhibitor PD98059: in vitro evaluation and pharmacokinetics.Drug delivery and translational research · 2021Article
- TNF-α-induced sympathetic excitation requires EGFR and ERK1/2 signaling in cardiovascular regulatory regions of the forebrain.American journal of physiology. Heart and circulatory physiology · 2021Article
- Effect of Renal Denervation on Cardiac Function and Inflammatory Factors in Heart Failure After Myocardial Infarction.Journal of cardiovascular pharmacology · 2020Article
- An Injectable Microparticle Formulation Provides Long-Term Inhibition of Hypothalamic ERK1/2 Activity and Sympathetic Excitation in Rats with Heart Failure.Molecular pharmaceutics · 2020Article
- Brain TACE (Tumor Necrosis Factor-α-Converting Enzyme) Contributes to Sympathetic Excitation in Heart Failure Rats.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Hypothalamic dysfunction in heart failure: pathogenetic mechanisms and therapeutic implications.Heart failure reviews · 2018Review
- The biochemical alterations underlying post-burn hypermetabolism.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- TNF-α receptor 1 knockdown in the subfornical organ ameliorates sympathetic excitation and cardiac hemodynamics in heart failure rats.American journal of physiology. Heart and circulatory physiology · 2017Article
- Article
- Disruption of calpain reduces lipotoxicity-induced cardiac injury by preventing endoplasmic reticulum stress.Biochimica et biophysica acta · 2016Article
- Endoplasmic reticulum stress increases brain MAPK signaling, inflammation and renin-angiotensin system activity and sympathetic nerve activity in heart failure.American journal of physiology. Heart and circulatory physiology · 2016Article
- FGF21 ameliorates the neurocontrol of blood pressure in the high fructose-drinking rats.Scientific reports · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitogen-activated protein kinase (MAPK) signaling and endoplasmic reticulum (ER) stress in the brain have been implicated in the pathophysiology of hypertension. This study determined whether ER stress occurs in subfornical organ and hypothalamic paraventricular nucleus in heart failure (HF) and how MAPK signaling interacts with ER stress and other inflammatory mediators. HF rats had significantly higher levels of the ER stress biomarkers (glucose-regulated protein 78, activating transcription factor 6, activating transcription factor 4, X-box binding protein 1, P58(IPK), and C/EBP homologous protein) in subfornical organ and paraventricular nucleus, which were attenuated by a 4-week intracerebroventricular infusion of inhibitors selective for p44/42 MAPK (PD98059), p38 MAPK (SB203580), or c-Jun N-terminal kinase (SP600125). HF rats also had higher mRNA levels of tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, and nuclear factor-κB p65, and a lower mRNA level of IκB-α, in subfornical organ and paraventricular nucleus, compared with SHAM rats, and these indicators of increased inflammation were attenuated in the HF rats treated with the MAPK inhibitors. Plasma norepinephrine level was higher in HF rats than in SHAM rats but was reduced in the HF rats treated with PD98059 and SB203580. A 4-week intracerebroventricular infusion of PD98059 also improved some hemodynamic and anatomic indicators of left ventricular function in HF rats. These data demonstrate that ER stress increases in the subfornical organ and paraventricular nucleus of rats with ischemia-induced HF and that inhibition of brain MAPK signaling reduces brain ER stress and inflammation and decreases sympathetic excitation in HF. An interaction between MAPK signaling and ER stress in cardiovascular regions of the brain may contribute to the development of HF.
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