Last update 01 Nov 2024

Phospholipids

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with Phospholipids

Bacterial biofilms inhibitors(University of South China)

Target

Phospholipids

Mechanism

Phospholipids inhibitors [+1]

Active Org.

University of South China

Originator Org.

University of South China

Active Indication

MRSA - Methicillin resistant Staphylococcus aureus infection

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Phospholipids

100 Translational Medicine associated with Phospholipids

0 Patents (Medical) associated with Phospholipids

Literatures (Medical) associated with Phospholipids

01 Aug 2021·AtherosclerosisQ2 · MEDICINE

Effects of empagliflozin on lipoprotein subfractions in patients with type 2 diabetes: data from a randomized, placebo-controlled study

Q2 · MEDICINE

Article

Author: Scharnagl, Hubert ; Korbinian Hartmann, Niels-Ulrik ; Marx, Nikolaus ; Lehrke, Michael ; Böhm, Michael ; Möllmann, Julia ; Rau, Matthias ; März, Winfried ; Wied, Stephanie ; Thiele, Kirsten

BACKGROUND AND AIMSSodium-glucose cotransporter-2 inhibitors, glucose-lowering drugs that increase urinary glucose excretion, have been shown to reduce CV events in patients with type 2 diabetes (T2D), despite the fact that these agents increase blood levels of the proatherogenic low density lipoprotein cholesterol (LDL-C). It has been hypothesized that hemoconcentration due to osmotic diuresis, effects on calculated LDL particle size, or a modulation of lipoprotein subfractions may play a role in this context but to date the underlying mechanisms remain largely unexplored. Therefore, the present study examined effects of empagliflozin on LDL-C and lipoprotein subfractions including calculated LDL particle size and composition.METHODSIn this placebo-controlled, randomized, double blind study, patients with T2D were randomized to empagliflozin 10 mg (n = 20) or placebo (n = 22). Composition of lipoprotein subfractions was assessed before and after 3 months of treatment. Lipoproteins were separated using a combined ultracentrifugation-precipitation method (β-quantification).RESULTSEmpagliflozin increased LDL-C after 3 months of treatment (from baseline: 103 ± 36 mg/dL to 112 ± 47 mg/dL; p < 0.001) while no difference was recorded after day 1 or day 3 of treatment. The increase of LDL-C was paralleled by an increase of total cholesterol (baseline: 169 ± 41 mg/dL, 3 months: 185 ± 48 mg/dL; p = 0.001). Analyses of lipoprotein subfractions revealed LDL phospholipids and LDL apolipoprotein B to be increased by empagliflozin after 3 months of treatment while calculated LDL particle size was not affected. In addition empagliflozin increased free fatty acid concentrations.CONCLUSIONSEmpagliflozin treatment of patients with T2D increased LDL-C and LDL apolipoprotein B levels but had no effect on calculated LDL particle size.

01 Jun 2021·AtherosclerosisQ2 · MEDICINE

Lysophosphatidylcholine in phospholipase A2-modified LDL triggers secretion of angiopoietin 2

Q2 · MEDICINE

Article

Author: Mäyränpää, Mikko I ; Korhonen, Emilia A ; Kovanen, Petri T ; Hakanpää, Laura ; Saharinen, Pipsa ; Alitalo, Kari ; Lorey, Martina B ; Nguyen, Su Duy ; Öörni, Katariina

BACKGROUND AND AIMSSecretory phospholipase A₂ (PLA₂) hydrolyzes LDL phospholipids generating modified LDL particles (PLA₂-LDL) with increased atherogenic properties. Exocytosis of Weibel-Palade bodies (WPB) releases angiopoietin 2 (Ang2) and externalizes P-selectin, which both play important roles in vascular inflammation. Here, we investigated the effects of PLA₂-LDL on exocytosis of WPBs.METHODSHuman coronary artery endothelial cells (HCAECs) were stimulated with PLA₂- LDL, and its uptake and effect on Ang2 release, leukocyte adhesion, and intracellular calcium levels were measured. The effects of PLA₂-LDL on Ang2 release and WPB exocytosis were measured in and ex vivo in mice.RESULTSExposure of HCAECs to PLA₂-LDL triggered Ang2 secretion and promoted leukocyte-HCAEC interaction. Lysophosphatidylcholine was identified as a critical component of PLA₂-LDL regulating the WPB exocytosis, which was mediated by cell-surface proteoglycans, phospholipase C, intracellular calcium, and cytoskeletal remodeling. PLA₂-LDL also induced murine endothelial WPB exocytosis in blood vessels in and ex vivo, as evidenced by secretion of Ang2 in vivo, P-selectin translocation to plasma membrane in intact endothelial cells in thoracic artery and tracheal vessels, and reduced Ang2 staining in tracheal endothelial cells. Finally, in contrast to normal human coronary arteries, in which Ang2 was present only in the endothelial layer, at sites of advanced atherosclerotic lesions, Ang2 was detected also in the intima, media, and adventitia.CONCLUSIONSOur studies reveal PLA₂-LDL as a potent agonist of endothelial WPB exocytosis, resulting in increased secretion of Ang2 and translocation of P-selectin. The results provide mechanistic insight into PLA₂-LDL-dependent promotion of vascular inflammation and atherosclerosis.

01 Jun 2010·Clinical ImmunologyQ3 · MEDICINE

C-reactive protein in myocardial infarction binds to circulating microparticles but is not associated with complement activation

Q3 · MEDICINE

Article

Author: R. Nieuwland ; R.J. de Winter ; A. Sturk ; P.M. van der Zee ; É. Biró ; C.E. Hack ; L.A. Trouw ; Y. Ko

BACKGROUNDC-reactive protein (CRP) is elevated in patients with acute myocardial infarction (AMI). When CRP binds to membrane phospholipids or Fc receptors, it activates the complement system. Recent studies show that CRP can be exposed on cell-derived microparticles (MP) and is associated complement activation.OBJECTIVESWe studied complement activation on circulating MP in AMI patients and healthy controls.METHODSMP were isolated from plasma of AMI patients (n=21) and sex- and age-matched healthy individuals (n=10), and analyzed by flow cytometry for bound complement components (C1q, C4, C3) and complement inhibitor and activator molecules (C4bp, CRP, serum amyloid P component, immunoglobulins IgM and IgG). Concurrently, the levels of fluid phase complement activation products and inhibitor and activator molecules were determined.RESULTSFluid phase CRP, MP with bound CRP (CRP + MP), and C3 activation products were elevated in AMI patients compared to controls (P=0.032, P=0.031 and P=0.023, respectively), and fluid phase CRP correlated with CRP+ MP (r=0.84, P<0.001). Although CRP+ MP were elevated, they were not associated with C1q+ MP (r=0.32, P=0.174). In contrast, IgG+ MP were associated with C1q+ MP (r=0.73, P<0.001), C4+ MP and C3+ MP (r=0.78 and r=0.87, respectively; both P<0.001), and C4bp (r=0.63, P=0.004). In healthy individuals, CRP+ MP were strongly associated with C1q+ MP (r=0.82, P=0.007), which in turn were associated with C4+ MP and C3+ MP (r=0.68, P=0.032 and r=0.68, P=0.031, respectively).CONCLUSIONSDespite CRP-associated complement activation on the surface of MP in healthy individuals and a strong correlation between MP-bound CRP and fluid phase CRP in AMI patients, the MP-associated complement activation is IgG- but not CRP-dependent in AMI patients.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

Phospholipids

Basic Info

Related

Analysis