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Engineering synthetic signaling receptors to enable erythropoietin-free erythropoiesis.
Nat Commun
January 2025
Department of Surgery, University of California, San Francisco, San Francisco, CA, USA.
Blood transfusion plays a vital role in modern medicine, but frequent shortages occur. Ex vivo manufacturing of red blood cells (RBCs) from universal donor cells offers a potential solution, yet the high cost of recombinant cytokines remains a barrier. Erythropoietin (EPO) signaling is crucial for RBC development, and EPO is among the most expensive media components.
View Article and Find Full Text PDFCarbon monoxide alleviates endotoxin-induced acute lung injury via NADPH oxidase inhibition in macrophages and neutrophils.
Biochem Pharmacol
January 2025
Division of Pharmacodynamics, Faculty of Pharmacy, Keio University, Tokyo, Japan. Electronic address:
Sepsis is a life-threatening condition caused by severe infection and often complicates acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) due to the collapse of the oxidative and inflammatory balance induced by microbial pathogens, including lipopolysaccharides (LPS). In sepsis-related ARDS/ALI, NADPH oxidase (NOX) and toll-like receptors (TLR) in neutrophils and macrophages are key players in initiating oxidative and inflammatory imbalances. Although NOX and TLR activation has been linked to carbon monoxide (CO), the mechanism by which CO affects sepsis-related ARDS/ALI through NOX and TLR remains unknown.
View Article and Find Full Text PDFGlucocorticoid pre-administration improves LNP-mRNA mediated protein replacement and genome editing therapies.
Int J Pharm
January 2025
Laboratory of Biotherapy, National Key Laboratory of Biotherapy, Cancer Center, West China Hospital, Sichuan University, Renmin Nanlu 17, Chengdu 610041, Sichuan, China. Electronic address:
Lipid nanoparticles (LNPs) are among the most promising non-viral mRNA delivery systems for gene therapeutic applications. However, the in vivo delivery of LNP-mRNA remains challenging due to multiple intrinsic barriers that hinder LNPs from reaching their target cells. In this study, we sought to enhance LNP delivery by manipulating intrinsic regulatory mechanisms involved in their metabolism.
View Article and Find Full Text PDFHS inhibition of xanthine dehydrogenase to xanthine oxidase conversion reduces uric acid levels and improves myoblast functions.
Biochim Biophys Acta Mol Cell Res
January 2025
School of Natural Sciences, Laurentian University, Sudbury, Canada; Cardiovascular and Metabolic Research Unit, Laurentian University, Sudbury, Canada. Electronic address:
Hydrogen sulfide (HS) is an important gasotransmitter that regulates a wide range of pathophysiological processes. Higher uric acid levels are associated with an increased risk of metabolic diseases. The causal mechanism linking HS signalling and uric acid metabolism in skeletal muscles has not yet been elucidated.
View Article and Find Full Text PDFA functional cardiac patch promotes cardiac repair by modulating the CCR2 cardiac-resident macrophage niche and their cell crosstalk.
Cell Rep Med
January 2025
Biomaterials Research Center, School of Biomedical Engineering, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China; Department of Cardiology, Guangzhou Institute of Cardiovascular Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, China; Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China; School of Basic Medical Science, Guangzhou Medical University, Guangzhou, Guangdong 510182, P.R. China. Electronic address:
C-C chemokine receptor type 2 (CCR2) cardiac-resident macrophages (CCR2 cRMs) are known to promote cardiac repair after myocardial infarction (MI). However, the substantial depletion and slow recovery of CCR2 cRMs pose significant barriers in cardiac recovery. Here, we construct a functional conductive cardiac patch (CCP) that can provide exogenously elastic conductive microenvironment and induce endogenously reparative microenvironment mediated by CCR2 cRMs for MI repair.
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