Results 31 to 40 of about 12,272 (191)
BackgroundCurrently, there are various lipid-lowering therapies in clinical practice, and the emergence of PCSK9 inhibitors has undoubtedly added a valuable tool to lipid-lowering strategies.
Qiang Niu, Qilei Wang, Feng Chen, Bo Li
doaj +1 more source
Background In addition to lowering cholesterol levels, the proprotein convertase subtilis kexin 9 (PCSK9) inhibitor has a variety of effects, including anti‐neuroapoptosis.
Qiang Huang, Qin Zhang, Bei Cao
doaj +1 more source
Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) have emerged as a therapeutic option for patients with hypercholesterolemia who do not attain low-density lipoprotein cholesterol (LDL-C) goals and/or are intolerant to other lipid-lowering drugs.
Juan, Vicente-Valor +9 more
openaire +2 more sources
Our experimental evidence supports a model in which ALO targets the HSPA8‐CMA‐ATP6V1A axis to induce lysosomal hyperacidification and initiate osmotic and lipidomic stress. These changes are associated with LMP and loss of lysosomal integrity in prostate cancer cells.
Bingzheng An +8 more
wiley +1 more source
PCSK9 Modulates Macrophage Polarization-Mediated Ventricular Remodeling after Myocardial Infarction
Background and Aims. An increasing number of high-risk patients with coronary heart disease (similar to acute myocardial infarction (AMI)) are using PCSK9 inhibitors.
Feifei Wang +5 more
doaj +1 more source
PCSK9 deficiency alters brain lipid composition without affecting brain development and function
PCSK9 induces lysosomal degradation of the low-density lipoprotein (LDL) receptor (LDLR) in the liver, hereby preventing removal of LDL cholesterol from the circulation.
Angela Pärn +22 more
doaj +1 more source
PCSK9 inhibitors for LDL lowering [PDF]
In 2003, families were described with a rare, autosomal dominant form of familial hypercholesterolemia due to gain-of-function mutations in proprotein convertase subtilisin/kexin type 9 (PCSK9) [1]. Subsequent studies demonstrated that PCSK9 is secreted from liver and accelerates degradation of LDL receptors [2,3].
openaire +2 more sources
USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis
This study reveals that USP5 drives vascular smooth muscle cell senescence and atherosclerosis by stabilizing TGFBR1, suppressing IDH2, and promoting glycolytic reprogramming, identifying the USP5‐TGFBR1‐IDH2 axis as a potential therapeutic target. ABSTRACT Vascular smooth muscle cell (VSMC) senescence contributes importantly to atherosclerotic plaque ...
Xinhai Cui +5 more
wiley +1 more source
PCSK9: NEW VICTORY AND HORIZONS
The review presents the latest data from the world scientific literature of clinical studies of inhibitors protoprotein convertasesubtilisin/kexin 9 type (PCSK9).
M. O. Smolina +3 more
doaj +1 more source
Self‑amplifying PCSK9–LOX‑1 feedback axis drives atherosclerotic progression by promoting oxLDL generation and endothelial uptake. A dual‑targeting nanoplatform (siPCSK9@PEAL NPs‑aL) is constructed to simultaneously silence hepatic PCSK9 for lipid lowering and block plaque LOX‑1 for anti‑inflammation.
Yi Duan +7 more
wiley +1 more source

