Filtered By:
Drug: Niacin

This page shows you your search results in order of date.

Order by Relevance | Date

Total 7 results found since Jan 2013.

Role of Lipoprotein(a) in Atherosclerotic Cardiovascular Disease: A Review of Current and Emerging Therapies
AbstractLipoprotein(a), or Lp(a), is structurally like low-density lipoprotein (LDL) but differs in that it contains glycoprotein apolipoprotein(a) [apo(a)]. Due to its prothrombotic and proinflammatory properties, Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis. Lp(a) levels are genetically determined, and it is estimated that 20-25% of the global population has an Lp(a) level ≥50 mg/dL (or ≥125 nmol/L). Diet and lifestyle interventions have little to no effect on Lp(a) levels. Lipoprotein apheresis is the only approved treatment for elevated Lp(a) but i...
Source: Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy - July 19, 2023 Category: Drugs & Pharmacology Authors: Ibrahim S. Alhomoud, Azita Talasaz, Anurag Mehta, Michael Kelly, Evan M. Sisson, John D. Bucheit, Roy Brown, Dave L. Dixon Tags: REVIEW Source Type: research

Inclisiran: A Novel Small Interfering RNA Drug for LDL Reduction
This article is protected by copyright. All rights reserved.PMID:35279835 | DOI:10.1002/jcph.2045
Source: The Journal of Clinical Pharmacology - March 13, 2022 Category: Drugs & Pharmacology Authors: Kimberly W Smith C Michael White Source Type: research

Nicotinic acid suppresses sebaceous lipogenesis of human sebocytes via activating hydroxycarboxylic acid receptor 2 (HCA2 ).
Abstract Nicotinic acid (NA) activates hydroxycarboxylic acid receptor 2 (HCA2 ), and it is widely used in treating dyslipidaemias. Since its side effects include skin dryness, whereas its deficiency can be accompanied by dyssebacia, characterized by sebaceous gland enlargement, we asked if HCA2 is expressed on human sebocytes, and if NA influences sebocyte functions. By using human immortalized SZ95 sebocytes, we found that non-cytotoxic (≤100 μmol/L; MTT-assay) concentrations of NA had no effect on the homeostatic sebaceous lipogenesis (SLG; Nile Red), but normalized excessive, acne-mimicking SLG induced by ...
Source: J Cell Mol Med - July 4, 2019 Category: Molecular Biology Authors: Markovics A, Tóth KF, Sós KE, Magi J, Gyöngyösi A, Benyó Z, Zouboulis CC, Bíró T, Oláh A Tags: J Cell Mol Med Source Type: research

Oxyresveratrol stimulates mucin production in an NAD+-dependent manner in human intestinal goblet cells.
In conclusion, OXY increases NAD+ levels, resulting in the stimulation of MUC2 expression in LS 174T cells. These findings present a novel role for NAD+ in stimulation of MUC2 expression. PMID: 29935245 [PubMed - as supplied by publisher]
Source: Food and Chemical Toxicology - June 20, 2018 Category: Food Science Authors: Hwang D, Jo H, Ma SH, Lim YH Tags: Food Chem Toxicol Source Type: research

Glutamate induces autophagy via the two-pore channels in neural cells.
In this study, we evaluated the effect of glutamate on autophagy in astrocytes at physiological, non-toxic concentration. We found that glutamate induces autophagy at similar extent as NAADP. By contrast, the NAADP antagonist NED-19 or SiRNA-mediated inhibition of TPC1/2 decreases autophagy induced by glutamate, confirming a role for NAADP in this pathway. The involvement of TPC1/2 in glutamate-induced autophagy was also confirmed in SHSY5Y neuroblastoma cells. Finally, we show that glutamate leads to a NAADP-dependent activation of AMPK, which is required for autophagy induction, while mTOR activity is not affected by thi...
Source: Oncotarget - January 6, 2017 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

CD38 Mediates Angiotensin II-induced Intracellular Ca(2+) Release in Rat Pulmonary Arterial Smooth Muscle Cells.
This study sought to characterize its roles in angiotension II (Ang II)-induced Ca2+ release (AICR) in PASMCs. Examination of CD38 expression in various rat arteries found high levels of CD38 mRNA and protein in pulmonary arteries. Ang II elicited Ca2+ response consisted of extracellular Ca2+ influx and intracellular Ca2+ release in PASMCs. AICR activated in the absence of extracellular Ca2+ was reduced by pharmacological or siRNA inhibition of CD38. It was also reduced by the cADPR-antagonist 8-bromo-cADPR or ryanodine; and by the NAADP-antagonist Ned-19 or disruption of endolysosomal Ca2+ stores with the vacuolar H+-ATPa...
Source: American Journal of Respiratory Cell and Molecular Biology - July 31, 2014 Category: Molecular Biology Authors: Lee S, Paudel O, Jiang Y, Yang XR, Sham JS Tags: Am J Respir Cell Mol Biol Source Type: research