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Patterns of C1-Inhibitor Plasma Levels and Kinin-Kallikrein System Activation in Relation to COVID-19 Severity.
Life (Basel)
November 2024
Department of Biomedical and Clinical Sciences, Università degli Studi di Milano, 20157 Milan, Italy.
Background: Although more than four years have passed since the pandemic began, SARS-CoV-2 continues to be of concern. Therefore, research into the underlying mechanisms that contribute to the development of the disease, especially in more severe forms, remains a priority. Sustained activation of the complement (CS), contact (CAS), and fibrinolytic and kinin-kallikrein systems (KKS) has been shown to play a central role in the pathogenesis of the disease.
View Article and Find Full Text PDFAlzheimer's Disease: In Vitro and In Vivo Evidence of Activation of the Plasma Bradykinin-Forming Cascade and Implications for Therapy.
Cells
December 2024
Astria Pharmaceuticals, Boston, MA 02210, USA.
The plaques associated with Alzheimer's disease are formed as a result of the aggregation of Aβ peptides, which vary in length from 38 to 43 amino acids. The 1-40 peptide is the most abundant, while the 1-42 peptide appears to be the most destructive to neurons and/or glial cells in a variety of assays. We have demonstrated that aggregated Aβ, a state prior to plaque formation, will activate the plasma bradykinin-forming pathway when tested in vitro.
View Article and Find Full Text PDFIdiopathic non-mast cell angioedema: Treatment insights from global experts.
Allergy Asthma Proc
January 2025
From the Division of Allergy and Immunology, Department of Medicine, University of California San Diego, La Jolla, California and.
Idiopathic non-mast cell angioedema (INMA) is a rare disease typified by recurrent attacks of cutaneous and subcutaneous swelling. Every attack carries the potential for severe morbidity and, in the case of laryngeal involvement, mortality. Whereas therapies approved for hereditary angioedema (HAE) have been used in the care of patients with INMA, little is known with regard to their efficacy for the treatment of this disease.
View Article and Find Full Text PDFA mechanistic model of in vitro plasma activation to evaluate therapeutic kallikrein-kinin system inhibitors.
PLoS Comput Biol
November 2024
CSL Ltd, Bio21 Institute, Melbourne, Victoria, Australia.
Background: The kallikrein-kinin system (KKS) is a complex biochemical pathway that plays a crucial role in regulating several physiological processes, including inflammation, coagulation, and blood pressure. Dysregulation of the KKS has been associated with several pathological conditions such as hereditary angioedema (HAE), hypertension, and stroke. Developing an accurate quantitative model of the KKS may provide a better understanding of its role in health and disease and facilitate the rapid and targeted development of effective therapies for KKS-related disorders.
View Article and Find Full Text PDFA novel assay of excess plasma kallikrein-kinin system activation in hereditary angioedema.
Front Allergy
September 2024
Takeda Development Center Americas Inc., Cambridge, MA, United States.
Article Synopsis
- Cleaved high-molecular-weight kininogen (HKa) serves as a biomarker for the activation of the kallikrein-kinin system (KKS) in patients with hereditary angioedema due to C1 inhibitor deficiency (HAE-C1INH).
- The study aimed to create an HKa-specific enzyme-linked immunosorbent assay (ELISA) for monitoring KKS activation in the blood of HAE-C1INH patients, utilizing a specific antibody found through phage display.
- Results showed that HKa levels were significantly higher in HAE-C1INH patients during attacks compared to healthy controls, indicating the potential of this ELISA for advancing drug development and understanding related diseases.
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