Results 71 to 80 of about 3,608 (158)
What's new? Endocrine drugs repurposed from treatment protocols are the primary medications available for breast cancer (BC) prevention in at‐risk women. Adverse effects, however, significantly minimize uptake and prevention impact. Here, the authors investigated licochalcone A (LicA), a non‐endocrine anti‐inflammatory agent with reported hematologic ...
Atieh Hajirahimkhan +14 more
wiley +1 more source
Abstract Alzheimer's disease (AD) is driven by interrelated pathologies, including the accumulation of amyloid β (Aβ), tau pathology, chronic neuroinflammation, and oxidative stress (OS). These pathological processes collectively lead to progressive neurodegeneration.
Zhengxiang Lv +5 more
wiley +1 more source
Prevention of Retinal Degeneration in a Rat Model of Smith-Lemli-Opitz Syndrome
Smith-Lemli-Opitz Syndrome (SLOS) is a recessive human disease caused by defective cholesterol (CHOL) synthesis at the level of DHCR7 (7-dehydrocholesterol reductase), which normally catalyzes the conversion of 7-dehydrocholesterol (7DHC) to CHOL ...
Steven J. Fliesler +6 more
doaj +1 more source
DHCR7: from sterol biosynthesis to oncogenic role in colorectal cancer [PDF]
Objective 7-Dehydrocholesterol reductase (DHCR7) is an enzyme that plays a crucial regulatory role in sterol biosynthesis and has been implicated in tumorigenesis and progression.
Chuan Zhou +8 more
doaj +2 more sources
RNA‐Binding Proteins and Ferroptosis in Cancer: Mechanism and Therapeutic Implications
Ferroptosis critically influences cancer cell fate and represents a promising therapeutic strategy. Emerging evidence identifies RNA‐binding proteins (RBPs) as key post‐transcriptional regulators of ferroptosis. The figure summarizes ferroptosis‐related RBPs across cancers: blue RBPs act as tumor suppressors by promoting ferroptosis, whereas red RBPs ...
Linlin Chang +6 more
wiley +1 more source
Elevated autophagy and mitochondrial dysfunction in the Smith–Lemli–Opitz Syndrome
Smith–Lemli–Opitz Syndrome (SLOS) is a congenital, autosomal recessive metabolic and developmental disorder caused by mutations in the enzyme which catalyzes the reduction of 7-dehydrocholesterol (7DHC) to cholesterol.
Shaohua Chang +7 more
doaj +1 more source
Lifespan‐Extending Endogenous Metabolites
Endogenous metabolites act as mediators of longevity by modulating conserved cellular pathways. We summarize mechanistic evidence linking specific metabolites to lifespan and healthspan benefits across model systems, with discussion of clinical evidence, translational opportunities, and remaining knowledge gaps.
Yizhou Jiang, Jing‐Dong J. Han
wiley +1 more source
Abstract In the context of current global change, variations in water temperature are one of the environmental conditions with serious consequences for marine life, including reproductive processes. In the small spotted catshark Scyliorhinus canicula, spermatogenesis occurs in spermatocysts composed of synchronously developing germ cells associated ...
Fabian Jeanne +4 more
wiley +1 more source
Cholesterol Deficiency Directs Autophagy‐Dependent Secretion of Extracellular Vesicles
Inhibition of cholesterol biosynthesis within models of rare disease and cancer causes increased release of small extracellular vesicles (sEVs) with distinct biological properties. Mechanistically, cholesterol depletion leads to impaired autophagic flux, redirection of autophagosomes to late endosomes, and subsequently increased sEV secretion ...
Jazmine D. W. Yaeger +6 more
wiley +1 more source
The use of the Dhcr7 knockout mouse to accurately determine the origin of fetal sterols
Mice with a targeted mutation of 3β-hydroxysterol Δ7-reductase (Dhcr7) that cannot convert 7-dehydrocholesterol to cholesterol were used to identify the origin of fetal sterols.
G.S. Tint +4 more
doaj +1 more source

