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Condition: Hypertension

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Total 587 results found since Jan 2013.

Zi Shen Huo Luo Formula Prevents Aldosterone-Induced Cardiomyocyte Hypertrophy and Cardiac Fibroblast Proliferation by Regulating the Striatin-Mediated MR/EGFR/ERK Signaling Pathway.
In conclusion, ZSHLF inhibits the downstream EGFR/ERK signaling pathway by blocking the striatin-mediated membrane localization of MR, which may be an important molecular mechanism by which ZSHLF improves aldosterone-induced myocardial remodeling. PMID: 33014117 [PubMed]
Source: Evidence-based Complementary and Alternative Medicine - October 7, 2020 Category: Complementary Medicine Tags: Evid Based Complement Alternat Med Source Type: research

Endothelial BMPR2 Loss Drives a Proliferative Response to BMP (Bone Morphogenetic Protein) 9 via Prolonged Canonical Signaling.
CONCLUSIONS: BMPR2 loss reverses the endothelial response to BMP9, causing enhanced proliferation. This finding has potential implications for the proposed translation of BMP9 as a treatment for pulmonary arterial hypertension and suggests the need for focused patient selection in clinical trials. PMID: 32998516 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - September 30, 2020 Category: Cardiology Authors: Theilmann AL, Hawke LG, Hilton LR, Whitford MKM, Cole DV, Mackeil JL, Dunham-Snary KJ, Mewburn J, James PD, Maurice DH, Archer SL, Ormiston ML Tags: Arterioscler Thromb Vasc Biol Source Type: research

TIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension.
CONCLUSIONS: TIGAR suppressed the proliferation and migration of PASMCs via inhibiting autophagy and ROS, and therefore, improved hypoxia-induced PH. Thus, TIGAR might be a promising therapeutic target for PAH. PMID: 32946259 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Heart and Circulatory Physiology - September 17, 2020 Category: Physiology Authors: Yamanaka R, Hoshino A, Fukai K, Urata R, Minami Y, Honda S, Fushimura Y, Hato D, Iwai-Kanai E, Matoba S Tags: Am J Physiol Heart Circ Physiol Source Type: research

Nitric oxide activates AMPK by modulating PDE3A in human pulmonary artery smooth muscle cells
Nitric oxide treatment increased PDE3A protein expression and PDE3 activity with a concomitant decrease in cAMP concentrations and increase in AMPK phosphorylation in human pulmonary artery smooth muscle cells. Knockdown of PDE3A using siRNA transfection blunted the NO ‐induced AMPK activation, indicating that PDE3A plays an important role in AMPK regulation in hPASMC. We speculate that NO‐induced increases in PDE3A and AMPK may have implications in the pathogenesis of pulmonary hypertensive disorders. AbstractPhosphodiesterase 3 (PDE3), of which there are two isoforms, PDE3A and PDE3B, hydrolyzes cAMP and cGMP —cycl...
Source: Physiological Reports - September 9, 2020 Category: Physiology Authors: Julie Dillard, Xiaomei Meng, Leif Nelin, Yusen Liu, Bernadette Chen Tags: ORIGINAL RESEARCH Source Type: research

Periostin: A Potential Therapeutic Target For Pulmonary Arterial Hypertension?
Conclusions: Our study reveals that POSTN expression is increased in human and animal models of PH and fosters PH development via a positive feedback loop between HIF-1α and POSTN during hypoxia. We propose that manipulating POSTIN expression may be an efficacious therapeutic target in the treatment of PH. Our results also suggest that POSTN may serve as a biomarker to estimate the severity of PH. PMID: 32752980 [PubMed - as supplied by publisher]
Source: Circulation Research - August 4, 2020 Category: Cardiology Authors: Nie X, Shen C, Tan J, Wu Z, Wang W, Chen Y, Dai Y, Yang X, Ye S, Chen J, Bian JS Tags: Circ Res Source Type: research

Sphingosine-1-phosphate promotes pulmonary artery smooth muscle cells proliferation by stimulating autophagy-mediated E-cadherin/CDH1 down-regulation.
Abstract It has been shown that sphingosine-1-phosphate (S1P) is elevated in patients with pulmonary arterial hypertension (PAH) and promotes the proliferation of pulmonary artery smooth muscle cells (PASMCs). Meanwhile, S1P has been found to induce the activation of autophagy in several types of human diseases including cancers. However, it is still unclear whether activation of autophagy mediates S1P-induced PASMCs proliferation, and detailed mechanisms responsible for these processes are indefinite. The aims of this study are to address these issues. S1P dose- and time-dependently reduced the expression of E-ca...
Source: European Journal of Pharmacology - July 9, 2020 Category: Drugs & Pharmacology Authors: Zhai C, Feng W, Shi W, Wang J, Zhang Q, Yan X, Wang Q, Li S, Liu L, Pan Y, Zhu Y, Chai L, Li C, Liu P, Chen Y, Li M Tags: Eur J Pharmacol Source Type: research

Salt causes aging-associated hypertension via vascular Wnt5a under Klotho deficiency
Aging is associated with a high prevalence of hypertension due to elevated susceptibility of BP to dietary salt, but its mechanism is unknown. Serum levels of Klotho, an anti-aging factor, decline with age. We found that high salt (HS) increased BP in aged mice and young heterozygous Klotho-knockout mice and was associated with increased vascular expression of Wnt5a and p-MYPT1, which indicate RhoA activity. Not only the Wnt inhibitor LGK974 and the Wnt5a antagonist Box5 but Klotho supplementation inhibits HS-induced BP elevation, similarly to the Rho kinase inhibitor fasudil, associated with reduced p-MYPT1 expression in ...
Source: Journal of Clinical Investigation - June 29, 2020 Category: Biomedical Science Authors: Wakako Kawarazaki, Risuke Mizuno, Mitsuhiro Nishimoto, Nobuhiro Ayuzawa, Daigoro Hirohama, Kohei Ueda, Fumiko Kawakami-Mori, Shigeyoshi Oba, Takeshi Marumo, Toshiro Fujita Source Type: research

Knockout of the Circadian Clock Protein PER1 Results in Sex-Dependent Alterations of ET-1 Production in Mice in Response to a High Salt Diet plus Mineralocorticoid Treatment.
Abstract Previously, we showed that global knockout (KO) of the circadian clock transcription factor PER1 in male, but not female, mice fed a high salt diet plus mineralocorticoid treatment (HS/DOCP) resulted in non-dipping hypertension and decreased night/day ratio of sodium (Na) excretion. Additionally, we have shown that the endothelin-1 (ET-1) gene is targeted by both PER1 and aldosterone. We hypothesized that ET-1 would exhibit a sex-specific response to HS/DOCP treatment in PER1 KO. Here we show that male, but not female, global PER1 KO mice exhibit a decreased night/day ratio of urinary ET-1. Gene expressio...
Source: Canadian Journal of Physiology and Pharmacology - May 20, 2020 Category: Drugs & Pharmacology Authors: Douma LG, Crislip GR, Cheng KY, Barral D, Masten S, Holzworth MR, Roig E, Glasford K, Beguiristain K, Li W, Bratanatawira P, Lynch IJ, Cain BD, Wingo CS, Gumz ML Tags: Can J Physiol Pharmacol Source Type: research

Extracellular adenosine enhances pulmonary artery vasa vasorum endothelium cell barrier function via the Gi/ELMO1/Rac1/PKA-dependent signaling mechanisms.
In this study we investigated in more detail the mechanisms linking Gi activation to downstream barrier protection pathways. Using a small interference RNA (siRNA) technique and Transendothelial Electrical Resistance (TER) assay, we found that the adaptor protein, ELMO1, the tyrosine phosphatase Shp2, and atypical Gi- and Rac-mediated PKA activation are implicated in VVEC barrier enhancement. In contrast, the actin-interacting GTP-binding protein, girdin and the PAK1 downstream target, LIM kinase, are not involved in this response. In addition, adenosine-dependent cytoskeletal rearrangement involves activation of cofilin a...
Source: Am J Physiol Cell Ph... - May 19, 2020 Category: Cytology Authors: Verin AD, Batori R, Kovacs-Kasa A, Cherian-Shaw M, Kumar S, Czikora I, Karoor V, Strassheim D, Stenmark KR, Gerasimovskaya E Tags: Am J Physiol Cell Physiol Source Type: research

LncRNA-Ang362 Promotes Pulmonary Arterial Hypertension by Regulating miR-221 and miR-222
Conclusion: Lnc-Ang362 played an important role in regulating the biological function of HPASMCs by promoting miR-221 and miR-222. Lnc-Ang362 thus may be a novel therapeutic lncRNA candidate for treating PAH.
Source: Shock - May 16, 2020 Category: Emergency Medicine Tags: Clinical Science Aspects Source Type: research

The diagnostic value and regulatory mechanism of miR-200a targeting ZEB1 in pregnancy-induced hypertension.
Conclusion: MiR-200a was upregulated in PIH patients, andinhibition of miR-200a may improve disease progression, as it could facilitatetrophoblastproliferation, migration and invasionandinhibitapoptosisby targeting ZEB1. PMID: 32345067 [PubMed - as supplied by publisher]
Source: Hypertension in Pregnancy - May 1, 2020 Category: OBGYN Tags: Hypertens Pregnancy Source Type: research

Effect of Aldosterone on Senescence and Proliferation Inhibition of Endothelial Progenitor Cells Induced by Sirtuin 1 (SIRT1) in Pulmonary Arterial Hypertension.
CONCLUSIONS ALDO promoted EPCs senescence and inhibited EPCs proliferation by downregulating SIRT1, which regulates the p53/p21 pathway, thus promoting PAH. PMID: 32303670 [PubMed - as supplied by publisher]
Source: Medical Science Monitor - April 20, 2020 Category: Research Tags: Med Sci Monit Source Type: research

TMEM16A regulates the cell cycle of pulmonary artery smooth muscle cells in high-flow-induced pulmonary arterial hypertension rat model.
In conclusion, TMEM16A may be involved in high pulmonary blood flow-induced PAH by regulating PASMC cell cycle progression. PMID: 32266023 [PubMed]
Source: Experimental and Therapeutic Medicine - April 10, 2020 Category: General Medicine Tags: Exp Ther Med Source Type: research

CARD9 promotes autophagy in cardiomyocytes in myocardial ischemia/reperfusion injury via interacting with Rubicon directly
AbstractAutophagy in cardiomyocyte is involved in myocardial ischemia/reperfusion (M-I/R) injury. Caspase recruitment domain-containing protein 9 (CARD9) plays a critical role in cardiovascular diseases (CVDs) such as hypertension and cardiac fibrosis. However, its role in autophagy following M-I/R injury is yet to be fully elucidated. Here, we found that CARD9 expression increased in M-I/R mouse hearts, and in H9c2 or neonatal rat ventricular myocytes (NRVMs) in response to hypoxia/reoxygenation (H/R) or H2O2. CARD9−/− mice exhibited a significant cardiac dysfunction following M-I/R injury (30  min of left ascending ...
Source: Basic Research in Cardiology - April 3, 2020 Category: Cardiology Source Type: research