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Condition: Thrombosis

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Total 185 results found since Jan 2013.

Endothelial < em > GNAQ < /em > p.R183Q Increases ANGPT2 (Angiopoietin-2) and Drives Formation of Enlarged Blood Vessels
CONCLUSIONS: Gαq-R183Q, when expressed in ECs, establishes constitutively active PLCβ3 signaling that leads to increased ANGPT2 and a proangiogenic, proinflammatory phenotype. EC-R183Q are sufficient to form enlarged CM-like vessels in mice, and suppression of ANGPT2 prevents the enlargement. Our study provides the first evidence that endothelial Gαq-R183Q is causative for CM and identifies ANGPT2 as a contributor to CM vascular phenotype.PMID:34670408 | DOI:10.1161/ATVBAHA.121.316651
Source: Arteriosclerosis, Thrombosis and Vascular Biology - October 21, 2021 Category: Cardiology Authors: Lan Huang Colette Bichsel Alexis Norris Jeremy Thorpe Jonathan Pevsner Sanda Alexandrescu Anna Pinto David Zurakowski Robin J Kleiman Mustafa Sahin Arin K Greene Joyce Bischoff Source Type: research

Group V Secretory Phospholipase A < sub > 2 < /sub > Regulates Endocytosis of Acetylated LDL by Transcriptional Activation of PGK1 in RAW264.7 Macrophage Cell Line
CONCLUSIONS: Nuclear sPLA2-V binds to the Pgk1 gene promoter region and increases its transcriptional activity. sPLA2-V regulates AcLDL endocytosis through PGK1-Beclin1 in a manner that is independent of its enzymatic activity in RAW264.7 cells.PMID:33775979 | DOI:10.5551/jat.62216
Source: Journal of Atherosclerosis and Thrombosis - March 29, 2021 Category: Cardiology Authors: Daisuke Fujioka Yosuke Watanabe Takamitsu Nakamura Takashi Yokoyama Keiji Miyazawa Makoto Murakami Kiyotaka Kugiyama Source Type: research

Targeting of antithrombin in hemophilia A or B with investigational siRNA therapeutic fitusiran - results of the phase 1 inhibitor cohort.
CONCLUSIONS: Monthly fitusiran was generally well tolerated, lowered antithrombin levels from baseline, and resulted in improved thrombin generation. These preliminary results suggest that monthly fitusiran treatment may reduce bleeding episodes and improve QoL in participants with hemophilia A or B with inhibitors. PMID: 33587824 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - February 15, 2021 Category: Hematology Authors: Pasi KJ, Lissitchkov T, Mamonov V, Mant T, Timofeeva M, Bagot C, Chowdary P, Georgiev P, Gercheva-Kyuchukova L, Madigan K, Nguyen H, Yu Q, Mei B, Benson CC, Ragni MV Tags: J Thromb Haemost Source Type: research

Truncated YY1 interacts with BASP1 through a 339KLK341 motif in YY1 and suppresses vascular smooth muscle cell growth and intimal hyperplasia after vascular injury
ConclusionThese studies identify a truncated form of YY1 (YY1B) that can interact with BASP1 and inhibit SMC proliferation, migration, and intimal hyperplasia after balloon injury of rat carotid arteries as effectively as full length YY1. We demonstrate the therapeutic potential of YY1B in vascular proliferative disease.
Source: Cardiovascular Research - January 28, 2021 Category: Cardiology Source Type: research

The Long Noncoding RNA RP11-728F11.4 Promotes Atherosclerosis.
CONCLUSIONS: RP11-728F11.4 promotes atherosclerosis, with an influence on cholesterol homeostasis and proinflammatory molecule production, thus representing a potential therapeutic target. PMID: 33406853 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - January 6, 2021 Category: Cardiology Authors: Dong XH, Lu ZF, Kang CM, Li XH, Haworth KE, Ma X, Lu JB, Liu XH, Fang FC, Wang CS, Ye JH, Zheng L, Wang Q, Ye S, Hu YW Tags: Arterioscler Thromb Vasc Biol Source Type: research

CROT (Carnitine O-Octanoyltransferase) Is a Novel Contributing Factor in Vascular Calcification via Promoting Fatty Acid Metabolism and Mitochondrial Dysfunction.
CONCLUSIONS: CROT is a novel contributing factor in vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction, as such CROT inhibition has strong potential as an antifibrocalcific therapy. PMID: 33356393 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - December 24, 2020 Category: Cardiology Authors: Okui T, Iwashita M, Rogers MA, Halu A, Atkins SK, Kuraoka S, Abdelhamid I, Higashi H, Ramsaroop A, Aikawa M, Singh SA, Aikawa E Tags: Arterioscler Thromb Vasc Biol Source Type: research

Endoplasmic Reticulum Stress Mediates Vascular Smooth Muscle Cell Calcification via Increased Release of Grp78-Loaded Extracellular Vesicles.
CONCLUSIONS: ER stress induces vascular calcification by increasing release of Grp78-loaded EVs. Our results reveal a novel mechanism of action of warfarin, involving increased EV release via the PERK-ATF4 pathway, contributing to calcification. This study is the first to show that warfarin induces ER stress and to link ER stress to cargo loading of EVs. PMID: 33297752 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - December 10, 2020 Category: Cardiology Authors: Furmanik M, van Gorp R, Whitehead M, Ahmad S, Bordoloi J, Kapustin A, Schurgers LJ, Shanahan CM Tags: Arterioscler Thromb Vasc Biol Source Type: research

Human Aortic Valve Interstitial Cells Display Proangiogenic Properties During Calcific Aortic Valve Disease.
CONCLUSIONS: We provide here the first proof of an angiogenic potential of human VICs isolated from patients with calcific aortic valve disease. These results point to a novel function of VICp in valve vascularization during calcific aortic valve disease, with a perivascular differentiation ability and a VEGF-A paracrine effect. Targeting perivascular differentiation and VEGF-A to slow calcific aortic valve disease progression warrants further investigation. PMID: 33147990 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - November 5, 2020 Category: Cardiology Authors: Gendron N, Rosa M, Blandinieres A, Sottejeau Y, Rossi E, Van Belle E, Idelcadi S, Lecourt S, Vincentelli A, Cras A, Jashari R, Chocron R, Baudouin Y, Pamart T, Bièche I, Nevo N, Cholley B, Rancic J, Staels B, Gaussem P, Dupont A, Carpentier A, Susen S, S Tags: Arterioscler Thromb Vasc Biol Source Type: research

Endothelial HMGB1 Is a Critical Regulator of LDL Transcytosis via an SREBP2-SR-BI Axis.
CONCLUSIONS: Endothelial HMGB1 regulates LDL transcytosis by prolonging the half-life of SREBP2, enhancing SR-BI expression. Translocation of HMGB1 to the nucleus in response to LDL requires SR-BI. PMID: 33054399 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - October 15, 2020 Category: Cardiology Authors: Ghaffari S, Jang E, Nabi FN, Sanwal R, Khosraviani N, Wang C, Steinberg BE, Goldenberg NM, Ikeda J, Lee WL Tags: Arterioscler Thromb Vasc Biol 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

Roles of microRNA-186 and vascular endothelial growth factor in hepatocellular carcinoma complicated with portal vein tumor thrombus.
In conclusion, VEGF was significantly increased in tumor thrombus and blood samples from HCC patients with vein tumor thrombus, which may be associated with the downregulation of miR-186. Thus, miR-186 may promote the development and progression of vein tumor thrombus in HCC. PMID: 32855736 [PubMed]
Source: Experimental and Therapeutic Medicine - August 30, 2020 Category: General Medicine Tags: Exp Ther Med Source Type: research

Knockdown of liver-derived factor XII by GalNAc-siRNA ALN-F12 prevents thrombosis in mice without impacting hemostatic function
Plasma coagulation Factor XII (FXII) plays a crucial role in contact activation, ultimately regulating both the kinin-kallikrein system and the intrinsic pathway of coagulation. A growing body of evidence suggests that inhibition of FXII can prevent thrombosis. Given FXII does not appear to modulate hemostasis, targeting FXII is a promising strategy for the prevention of pathological thrombus formation without the hemostatic risks typically associated with anticoagulants. To this end, a subcutaneously administered investigational RNAi therapeutic targeting liver F12 mRNA (ALN-F12) was developed.
Source: Thrombosis Research - August 26, 2020 Category: Hematology Authors: Jingxuan Liu, Brian C. Cooley, Akin Akinc, James Butler, Anna Borodovsky Tags: Full Length Article Source Type: research