Publications by authors named "J M Thurman"
Acute kidney injury (AKI) remains a major reason for hospitalization with limited therapeutic options. Although complement activation is implicated in AKI, the role of C5a receptor 1 (C5aR1) in kidney tubular cells is unclear. Herein, aristolochic acid nephropathy (AAN) and folic acid nephropathy (FAN) models were used to establish the role of C5aR1 in kidney tubules during AKI in germline C5ar1, myeloid cell-specific, and kidney tubule-specific C5ar1 knockout mice.
View Article and Find Full Text PDFActivation of platelets and the complement system in mice with -induced pulmonary hypertension.
Am J Physiol Lung Cell Mol Physiol
November 2024
Schistosomiasis-induced pulmonary hypertension (PH) presents a significant global health burden, yet the underlying mechanisms remain poorly understood. Here, we investigate the involvement of platelets and the complement system in the initiation events leading to -induced PH. We demonstrate that exposure leads to thrombocytopenia, platelet accumulation in the lung, and platelet activation.
View Article and Find Full Text PDFArticle Synopsis
- Uncontrolled activation of the complement system can lead to kidney damage in various diseases, notably affecting conditions like atypical hemolytic uremic syndrome and C3 glomerulopathy, with recent evidence linking it to diabetic nephropathy and other glomerulonephritides.
- In 2022, a conference organized by Kidney Diseases: Improving Global Outcomes (KDIGO) focused on the importance of complement dysregulation in kidney diseases, discussing its role in diagnosis and treatment strategies.
- Conference discussions highlighted patient concerns regarding genetic testing and the integration of new therapies, as well as the need for better understanding of biomarkers and the microenvironment of the kidneys to improve monitoring and treatment of these diseases.
Article Synopsis
- Complement-mediated diseases can be treated using specific inhibitors, but traditional systemic approaches may increase infection risk and have limited efficacy due to high levels of complement in circulation.
- Researchers developed a new therapy, an antibody fusion protein (C3d-mAb-2fH), that targets complement activity directly in affected tissues rather than systemic circulation, improving localized treatment.
- Experiments show that this approach effectively inhibits complement in tissue and has demonstrated positive results in models for skin and kidney diseases without causing systemic side effects.