LDLR (Low Density Lipoprotein Receptor)

Furthermore, in silico analyses demonstrated that high expression of FGFR1 was associated with high LDLR expression and clinicopathological features in PCa. Collectively, our data unveiled a previously unrecognized therapeutic avenue for CRPC by targeting FGFR1-driven cholesterol uptake and de novo synthesis.

Our findings underscore the superior cancer cell-killing capability of CAR-T cells. Additionally, CAR-macrophages play a crucial role in clearing cancer cells through phagocytosis, thereby synergistically supporting the activity of CAR-T cells.

We achieved normalization of circulating LDL cholesterol in two FH mouse models and prevention of atherosclerosis, even under high-fat diet challenge, without any long-term liver tumorigenicity. Overall, our in-depth assessment of the efficacy and safety of in vivo gene therapy for FH provides new insights into mechanisms of action and potential vulnerabilities, with implications for future developments of lipid-lowering gene therapies.

While most findings overlap with broader populations, this study underscores Cyprus's distinct genetic profile shaped by its complex demographic history. Our findings provide actionable insights for healthcare planning, support population-specific genomic screening programs development, and contribute to the global effort to refine precision medicine applications.

These findings collectively identify LDLRAD4 as a promising therapeutic target for MDS. However, its clinical applicability warrants further investigation to validate its potential.

We delineated LEMS as an enriched subset in LM and proposed targeting of LEMS-SPP1+ macrophage interactions as a therapeutic strategy to disrupt metastatic progression.

We further develop ancestry adjustment using matching and inverse probability weighting as well as regression and doubly robust methods; we extend this to examine oligogenic burden in the lysosomal storage pathway in PD. The CP reveals an approach to address heterogeneity and is an extensible method for inference and discovery in complex disease genetics.

Our study reveals a survival mechanism in OSCC: cells enhance exogenous lipid utilization to bypass glutamine dependence. Combined inhibition of LDL uptake and PPARα signaling may overcome metabolic plasticity, providing a rationale for precision therapies targeting metabolic heterogeneity in OSCC.

Moreover, we found that the uptake of macrophage-derived EVs lacking apolipoprotein E (ApoE) by Huh7 cells was lower than that of control EVs, highlighting the role of ApoE as a facilitator of EV transfer from macrophages into Huh7 cells. Overall, our study highlights the intricate mechanisms underlying EV-mediated communication between macrophages and Huh7 cells during lipotoxicity and provides insight into the development of EV-based therapies for MASLD.

Our research suggests that periplocin may serve as a promising treatment for IVDD, offering anti-inflammatory benefits, preventing ECM degradation, and promoting ECM anabolism.

The highest uptake by these cells was associated with a decrease in viability to 63% and a slight reduction in the percentage of cells in S phase after 24-hour exposure. Stable complexes of antibody-functionalized B4C nanoparticles were successfully obtained, demonstrating increased tropism towards cancer cells overexpressing LDLR and EGFR.

LDLR-OTNs demonstrated receptor-mediated uptake and potent cytotoxicity in LDLR- and FAS- overexpressing breast cancer cells. These findings support LDLR-targeted nanoparticles as a promising approach for delivering FAS inhibitors to LDLR-rich tumours, meriting further investigation in targeted cancer therapy development.