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PM Exposure Induces Glomerular Hyperfiltration in Mice in a Gender-Dependent Manner.
Toxics
December 2024
Shanxi Key Laboratory of Coal-Based Emerging Pollutant Identification and Risk Control, Research Center of Environment and Health, College of Environment and Resource, Shanxi University, Taiyuan 030006, China.
As one of the most common air pollutants, fine particulate matter (PM) increases the risk of diseases in various systems, including the urinary system. In the present study, we exposed male and female C57BL/6J mice to PM for 8 weeks. Examination of renal function indices, including creatinine (CRE), blood urea nitrogen (BUN), uric acid (UA), and urinary microalbumin, indicated that the kidneys of female mice, not male mice, underwent early renal injury, exhibiting glomerular hyperfiltration.
View Article and Find Full Text PDFBradykinin attenuates NiSO-induced autophagy in MIN6 cells and protects islet function in mice by regulating the PI3K/AKT/mTOR signaling pathway.
Biochem Biophys Res Commun
December 2024
Department of Endocrinology and Metabolism, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People's Republic of China; The Second Clinical Medical College, Lanzhou University, Lanzhou, People's Republic of China. Electronic address:
Previous studies have shown that nickel sulfate (NiSO) increases autophagy in thyroid cells and tissues. As an important organ of the endocrine system, the pancreas not only contributes to the exocrine function of digestion but also has the endocrine function of regulating blood sugar. However, it remains unknown whether NiSO increases pancreatic autophagy.
View Article and Find Full Text PDFObjective: Aim: To analyze the mechanisms of regulation of the body's proteolytic systems during inflammation, detection of inflammation markers in blood and prostate secretions in the experimental benign prostatic hyperplasia in rats.
Patients And Methods: Materials and Methods: The study was conducted on 30 male rats on the model of benign prostatic hyperplasia. Rats were randomized as following: the 1st group (n=6) - intact animals; the 2nd group (n=24) - rats with benign prostatic hyperplasia.
A 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 PDFNovel Insights into the Kallikrein-Kinin System in Fulminant Myocarditis: Physiological Basis and Potential Therapeutic Advances.
J Inflamm Res
October 2024
Department of Anesthesiology, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Fulminant myocarditis (FM) is characterized by rapid cardiac deterioration often instigated by an inflammatory cytokine storm. The kallikrein-kinin system (KKS) is a metabolic cascade known for releasing vasoactive kinins, such as bradykinin-related peptides, possessing diverse pharmacological activities that include inflammation, regulation of vascular permeability, endothelial barrier dysfunction, and blood pressure modulation. The type 1 and type 2 bradykinin receptors (B1R and B2R), integral components of the KKS system, mediate the primary biological effects of kinin peptides.
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