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Identification of genetic variants of the gene in association with COPD susceptibility.
Ann Med
December 2025
Department of General Practice, Hainan affiliated Hospital of Hainan Medical University, Hainan General Hospital, Haikou, China.
Background: Although existing studies have identified some genetic loci associated with chronic obstructive pulmonary disease (COPD) susceptibility, many variants remain to be discovered. The aim of this study was to further explore the potential relationship between single nucleotide polymorphisms (SNPs) and COPD risk.
Methods: Nine hundred and ninety-six subjects were recruited (498 COPD cases and 498 healthy controls).
CD209d/e promotes inflammation and lung injury during influenza virus infection.
Immunohorizons
January 2025
Division of Pulmonary Medicine, Department of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Influenza virus infects millions each year, contributing greatly to human morbidity and mortality. Upon viral infection, pathogen-associated molecular patterns activate pattern recognition receptors on host cells, triggering an immune response. The CD209 protein family, homologs of DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin), is thought to modulate immune responses to viruses.
View Article and Find Full Text PDFHepatic Estrogen Receptor Alpha Overexpression Protects Against Hepatic Insulin Resistance and MASLD.
Pathophysiology
January 2025
Department of Physiology, Ribeirão Preto School of Medicine, University of São Paulo, Ribeirão Preto 14049-900, Brazil.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with cardiometabolic risk. Although studies have shown that estradiol positively contributes to energy metabolism via estrogen receptor alpha (ERα), its role specifically in the liver is not defined. Therefore, this study aimed to evaluate the effects of ERα overexpression, specifically in the liver in mice fed a high-fat diet (HFD).
View Article and Find Full Text PDFLoss of Type 2 Bone Morphogenetic Protein Receptor Activates NOD-Like Receptor Family Protein 3/Gasdermin E-Mediated Pyroptosis in Pulmonary Arterial Hypertension.
J Am Heart Assoc
January 2025
The Center for Vascular Disease and Translational Medicine, The Third Xiangya Hospital Central South University Changsha Hunan China.
Background: Pulmonary arterial hypertension (PAH) is an incurable disease initiated by endothelial dysfunction, secondary to vascular inflammation and occlusive pulmonary arterial vascular remodeling, resulting in elevated pulmonary arterial pressure and right heart failure. Previous research has reported that dysfunction of type 2 bone morphogenetic protein receptor (BMPR2) signaling pathway in endothelium is inclined to prompt inflammation in PAH models, but the underlying mechanism of BMPR2 deficiency-mediated inflammation needs further investigation. This study was designed to investigate whether BMPR2 deficiency contributes to pulmonary arterial hypertension via the NLRP3 (NOD-like receptor family protein 3)/GSDME (gasdermin E)-mediated pyroptosis pathway.
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