Space travel is a growing area of interest and includes initiatives such as NASA's Moon-to-Mars Mission. Reports on the cardiovascular effects of space travel reveal changes in morphology, metabolism, and function of the cardiovascular system. In this study, the cardiovascular response to immunization in space was studied in mice which were housed and immunized while on the International Space Station (ISS). Mice were immunized with tetanus toxoid combined with the adjuvant CpG (TT + CpG) and the effects of vaccination in space were studied using transcriptomics. Analysis of the mouse heart transcriptome was performed on flight control and flight-immunized mice. The results show that immunization aboard the ISS stimulates heightened inflammation in the heart via induction of the nuclear factor kappa B (NF-κB) signaling pathway to promote the release of the pro-inflammatory cytokines IFNγ, IL-17 and IL-6. Additional transcriptomic changes included alterations in the cytoskeleton and in the expression of transcripts associated with protection from oxidative stress. In summary, inflammation in the heart can occur following immunization in space. This investigation explores the impact of immune challenges on the heart and lays the groundwork for future research into additional cardiac alterations which can occur during spaceflight.
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http://dx.doi.org/10.1186/s12864-025-11426-y | DOI Listing |
Sci Adv
March 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Randall Centre for Cell and Molecular Biophysics and British Heart Foundation Centre of Research Excellence, New Hunt's House, Guy's Campus, King's College London, London SE1 1UL, United Kingdom.
Muscle contraction is driven by myosin motors from the thick filaments pulling on the actin-containing thin filaments of the sarcomere, and it is regulated by structural changes in both filaments. Thin filaments are activated by an increase in intracellular calcium concentration [Ca] and by myosin binding to actin. Thick filaments are activated by direct sensing of the filament load.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
March 2025
MaineHeath Institute for Research, Center for Molecular Medicine, Scarborough, Maine, United States.
Obesity is a global health challenge associated with significant metabolic and cardiovascular risks. Bariatric surgery and GLP-1 receptor agonists (GLP-1RAs) are effective interventions for weight loss and metabolic improvement, yet their comparative effects on systemic metabolism-particularly energy metabolism, bone health, and heart function-remain unclear. In this study, obese male mice underwent vertical sleeve gastrectomy (VSG), 6 weeks of GLP-1RA (semaglutide) treatment, or sham procedure with saline injection as controls.
View Article and Find Full Text PDFGeroscience
March 2025
Department of Medicine, College of Human Medicine, Michigan State University, 1355 Bogue St, East Lansing, MI, 48824, USA.
Transient receptor potential ankyrin 1 (TRPA1) is a sensory channel expressed in vagal afferent nerves that detect noxious stimuli. Trpa1 knockout accelerates age-related cardiac fibrosis and dysfunction in mice. This study investigated whether TRPA1 activation with its selective agonist, allyl isothiocyanate (AITC), prevents cardiac aging.
View Article and Find Full Text PDFPurinergic Signal
March 2025
Division of Cardiology, Department of Medicine Solna, Karolinska Institutet, Solna, Stockholm, 17177, Sweden.
Atherosclerosis, a chronic inflammatory disease driven by lipid deposition and immune cell activation, remains a leading cause of cardiovascular morbidity and mortality. Emerging evidence highlights the role of purinergic signalling in atherogenesis, particularly the P2Y receptor in macrophages [1]. Using RNA sequencing, proteomics, expression and functional validation in cells, mouse models and human materials, this study provides comprehensive mechanistic insights into how macrophage P2Y receptors contribute to foam cell formation and plaque development through the phospholipase Cβ (PLCβ)/store-operated Ca entry/calreticulin/scavenger receptor A (SR-A) pathway.
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