LRP1 (LDL Receptor Related Protein 1)

Crucially, ANG showed no signal retention in glioma or brain metastasis models despite their high vascular permeability and LRP1 expression, effectively ruling out the possibility that the signal in PFF rats is driven by non-specific leakage or the enhanced permeability and retention (EPR) effect. These findings demonstrate that ANG is a promising CEST contrast agent for visualizing α-synuclein deposits in the PFF-induced rat model, providing a potential foundation for translational imaging studies in PD.

Notably, in ex vivo human GBM specimens, ANG-hCy-MC achieved a remarkable tumor-to-normal fluorescence ratio of 7.83 at the invasive edge, enabling clear identification of even single infiltrating tumor cells. This probe allows real-time, high-contrast intraoperative guidance with unprecedented resolution, offering a powerful and clinically translatable strategy for achieving complete tumor resection and improved patient outcomes in GBM surgery.

Estradiol administration in androgen‑deprived male mice produces a constellation of metabolic derangements-including enhanced hepatic gluconeogenesis, impaired TG clearance, and inflammatory adipocyte hypertrophy-that likely underlie the increased CVD risk observed clinically. The identified molecular nodes (PEPCK, hepatic lipase, LRP1, LDLR, MTP, and adipose‑macrophage TNFα) provide potential targets for mitigating estrogen‑induced CVD risk while preserving its therapeutic benefit for PrCa.

Recent advances, including in silico optimization, in vivo SELEX, BBB chip-based MPS-SELEX, and nanoparticle-aptamer hybrids, have identified brain-penetrating aptamers and enhanced the brain delivery efficiency. This review highlights the potential of aptamers to transform CNS-targeted therapies.

Finally, we review translational opportunities and challenges, including candidate biomarkers (tumor MDK by IHC/RNA and circulating MDK by ELISA) and rational combination strategies that pair MDK blockade with MAPK-pathway inhibitors or PD-1/PD-L1 immunotherapy. Collectively, these data position MDK as a tractable node connecting tumor-intrinsic signaling with stromal and immune regulation.

Integrated analysis highlighted key miRNA-protein interaction networks, identifying hsa-miR-1-3p and LRP1 as potential diagnostic biomarkers, and their differential expression was further confirmed by reverse transcription-quantitative PCR. These findings provide novel insights into the role of EVs in CC pathogenesis and offer promising potential targets for early diagnosis and therapeutic intervention.

Additionally, its involvement in treatment resistance and potential applications in drug delivery for brain tumors are discussed. This review aims to provide a theoretical basis for the development of LRP1 as a novel therapeutic target in cancer treatment and its potential translation into precision medicine.

Targeting the MDK/LRP1 axis with Resmetirom offers a promising therapeutic strategy for MASH-associated HCC, addressing both metabolic dysfunction and tumor progression.

We propose combining MDK blockade with MEK, SHP2, or immune checkpoint inhibitors, using serum MDK and phospho-signaling as pharmacodynamic markers. We emphasize the near‑term opportunity in NF1‑OPG and MPNST while drawing lessons from NF1‑altered tumors outside the nervous system that reinforce combination strategies for neuro‑oncology.

Increasing knowledge of HPX biology will elucidate the causes that regulate plasma HPX, thus improving clinical and veterinary care. Interestingly, increased understanding of the hematological adaptations to weightlessness that lead to anemia, termed "space anemia," in astronauts and space tourists may provide new insights into HPX's role in maintaining iron homeostasis and red cell biology under microgravity conditions as well as upon recovery from space and other anemias.

This post-transcriptional regulation led to significant LRP1 suppression, subsequently inhibiting proliferation and restoring chemosensitivity. Our findings establish a novel piRNA-guided mechanism for overcoming chemoresistance and suggest that targeting the piR-43452/GTSF1/PIWIL4/LRP1 axis may provide therapeutic benefit in gemcitabine-resistant BCa.

LRP1 may act as an important molecule in modulating communication between pancreatic cancer cells and neural tissues. Our study offers new potential targets for the treatment of pancreatic cancer neural invasion.