Purpose: The purpose of this review was to examine the role of IL-1β in the inflammatory process central to the development of atherosclerosis and to discuss current clinical evidence for treatments targeting IL-1β in coronary artery disease.
Recent Findings: IL-1β has been shown to modulate atherosclerotic plaque progression by upregulating the synthesis of adhesion molecules on endothelial cells, as well increasing activation and proliferation of vascular smooth muscle cells. Animal studies have further suggested that alterations in the balance between agonists and antagonists of IL-1β are important in promoting atherosclerosis. In humans, preliminary assessment of therapy targeting IL-1β noted early reductions in serum inflammatory biomarkers among those with systemic inflammatory or coronary artery disease. The CANTOS trial, a large randomized double-blind study found that canakinumab, a monoclonal antibody targeting IL-1β, reduced ischemic events in patients being treated for secondary prevention. Cellular, animal, and now clinical studies have suggested a role for therapies aimed at IL-1β for treatment of CAD. However, given potential side effects and costs of these medications, further study is required to determine which patients may be most suited for treatment above current standard of care.
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http://dx.doi.org/10.1007/s11883-018-0754-6 | DOI Listing |
Mol Biol Cell
January 2025
Department of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
β-tubulin isotypes exhibit similar sequences but different activities, suggesting that limited sequence divergence is functionally important. We investigated this hypothesis for TUBB3/β3, a β-tubulin linked to aggressive cancers and chemoresistance in humans. We created mutant yeast strains with β-tubulin alleles that mimic variant residues in β3 and find that residues at the lateral interface are sufficient to alter microtubule dynamics and response to microtubule targeting agents.
View Article and Find Full Text PDFACS Chem Biol
January 2025
Department of Chemistry, Binghamton University, the State University of New York, Binghamton, New York 13902, United States.
RNA interference (RNAi) has rapidly matured as a novel therapeutic approach. In this field, chemical modifications have been critical to the clinical success of short interfering RNAs (siRNAs). Notwithstanding the significant advances, achieving robust durability and gene silencing in extrahepatic tissues, as well as reducing off-target effects of siRNA, are areas where chemical modifications can still improve siRNA performance.
View Article and Find Full Text PDFJAMA Netw Open
January 2025
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Importance: Lung cancer in individuals who have never smoked (INS) is a growing global concern, with a rapidly increasing incidence and proportion among all lung cancer cases. Particularly in East Asia, opportunistic lung cancer screening (LCS) programs targeting INS have gained popularity. However, the sex-specific outcomes and drawbacks of screening INS remain unexplored, with data predominantly focused on women.
View Article and Find Full Text PDFCell Biochem Biophys
January 2025
Department of Otolaryngology, Head and Neck Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, China.
Sensorineural hearing loss (SNHL) is an increasingly prevalent sensory disorder, but the underlying mechanisms remain poorly understood. Adaptor related protein complex 2 subunit beta 1 (AP2B1) has been indicated to be detectable in mature cochleae. Nonetheless, it is unclear whether AP2B1 is implicated in the progression of SNHL.
View Article and Find Full Text PDFJ Cardiovasc Transl Res
January 2025
Department of Vascular and Endovascular Surgery, Changzheng Hospital, Affiliated to the Naval Medical University, Shanghai, 200003, China.
CHI3L1 is strongly associated with atherosclerosis, but its role in macrophages remains unknown. In this study, we observed a significant up-regulation of CHI3L1 in both carotid plaques and serum of symptomatic patients, and demonstrated that CHI3L1 impairs the efferocytosis of macrophages by down-regulating crucial efferocytic mediator MFGE8 through inhibiting ATF2, which binds directly to the enhancer of MFGE8. In human plaques, we observed a negative correlation between CHI3L1 expression and both ATF2 and MFGE8 levels, further proved their involvement in plaque destabilization.
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