Results 221 to 230 of about 37,789 (262)

Prelamin A in an <i>Lmna</i> <sup>L648R/L648R</sup> Mouse Model Does Not Promote Atherosclerosis or Vascular Smooth Muscle Loss. [PDF]

open access: yesArterioscler Thromb Vasc Biol
Wang Y   +6 more
europepmc   +1 more source

Regulation of intestinal LDLR by the LXR-IDOL axis [PDF]

open access: yesAtherosclerosis, 2020
Background and aims: Cholesterol metabolism is tightly regulated by transcriptional and post-transcriptional mechanisms. Accordingly, dysregulation of cholesterol metabolism is a major risk factor for the development of coronary artery disease and ...
Noam Zelcer   +2 more
exaly   +5 more sources

Triciribine increases LDLR expression and LDL uptake through stabilization of LDLR mRNA

open access: yesScientific Reports, 2018
AbstractLow-density lipoprotein receptor (LDLR) is a key regulator of the metabolism of plasma low-density lipoprotein cholesterol (LDL-C), the elevated levels of which are associated with an increased risk of cardiovascular disease. Therefore, enhancing LDLR expression represents a potent treatment strategy for hypercholesterolemia.
Katrine Bjune
exaly   +3 more sources

Akt2/LDLr double knockout mice display impaired glucose tolerance and develop more complex atherosclerotic plaques than LDLr knockout mice

open access: yesCardiovascular Research, 2014
To characterize the phenotype of Akt2/low-density-lipoprotein receptor double knockout (dKO) (Akt2/LDLr dKO) mice with respect to insulin resistance and features of atherosclerotic plaque progression.
Dallinga-Thie G M   +2 more
exaly   +2 more sources

Berberine-induced LDLR up-regulation involves JNK pathway

open access: yesBiochemical and Biophysical Research Communications, 2007
Berberine, an herbal alkaloid, has been reported to have a lipid lowering effect by stabilizing hepatic LDLR mRNA in an ERK-dependent manner rather than promoting transcriptional activity.
Yangsoo Jang   +2 more
exaly   +2 more sources

Analysis of LDLR variants from homozygous FH patients carrying multiple mutations in the LDLR gene

Atherosclerosis, 2017
Familial hypercholesterolemia (FH) is an autosomal dominant disease with widespread global prevalence that partially accounts for the high prevalence of premature coronary heart disease. Although the majority of research on FH has focused on single heterozygous LDLR mutations, there have been limited reports of double LDLR mutations on the same ...
Lu-Ya Wang   +2 more
exaly   +3 more sources

LDLR missense variants disturb structural conformation and LDLR activity in T-lymphocytes of Familial hypercholesterolemia patients

Gene, 2023
Familial hypercholesterolemia (FH) is caused by deleterious mutations in the LDLR that increase markedly low-density lipoprotein (LDL) cholesterol and cause premature atherosclerotic cardiovascular disease. Functional effects of pathogenic LDLR variants identified in Brazilian FH patients were assessed using in vitro and in silico studies.
Thais Kristini Almendros, Barbosa   +15 more
openaire   +2 more sources

AAV8- LDLR Gene Therapy in Ldlr -KO and Homozygous Ldlr p.W483X Mice

Human Gene Therapy
The low-density lipoprotein receptor (LDLR) plays a crucial role in cholesterol regulation and lipoprotein transport. Variations in the LDLR gene can cause familial hypercholesterolemia (FH), with homozygous familial hypercholesterolemia (HoFH) being the most severe form.
Qingao Li   +8 more
openaire   +2 more sources

Validation of LDLr Activity as a Tool to Improve Genetic Diagnosis of Familial Hypercholesterolemia: A Retrospective on Functional Characterization of LDLr Variants [PDF]

open access: yesInternational Journal of Molecular Sciences, 2018
Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by high blood-cholesterol levels mostly caused by mutations in the low-density lipoprotein receptor (LDLr). With a prevalence as high as 1/200 in some populations, genetic screening for pathogenic LDLr mutations is a cost-effective approach in families classified as ...
Helena Ostolaza   +2 more
exaly   +5 more sources

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