Objective: To investigate the relationship between matrix metalloproteinase 9 (MMP-9) gene polymorphism and the efficacy of glucocorticoid therapy in idiopathic pulmonary fibrosis (IPF) patients.
Methods: We conducted a case-control study. Between January 2013 and September 2014, 115 patients at the Nine Department of Respiratory Medicine, Nanjing Chest Hospital, diagnosed with IPF were enrolled to be the IPF group and 100 healthy subjects were enrolled to be the control group. Prednisone was used to treat IPF patients. Polymerase chain reaction-restriction fragment length polymorphism was used to identify MMP-9 1562C> T polymorphism. The Sandwich enzyme-linked immunosorbent assay was used to measure the serum level of MMP-9 and tissue inhibitor of metalloproteinases 1 (TIMP-1) in the IPF patients before and after the glucocorticoid treatment.
Results: The frequencies of the TT genotype and the T allele of MMP-9 1562C> T gene were found significantly higher in the IPF group compared with the control group (both p < 0.05). Serum levels of MMP-9 and TIMP-1 in IPF patients in each of the three genotype groups before glucocorticoid treatment were significantly higher than those in the control group (all p < 0.05). After the glucocorticoid treatment, MMP-9 and TIMP-1 levels decreased significantly compared with the levels before the glucocorticoid treatment in the IPF patients in each genotype group (all p < 0.05), but were still higher than those in the control group (all p < 0.05). The proportion of "remarkable effect" in the IPF patients of the CC genotype group was significantly higher than that in the other two genotype groups, while the rate of adverse reactions of the CC group was significantly lower than the other two groups (all p < 0.05).
Conclusion: MMP-9 gene 1562C> T polymorphism may affect the efficacy of the glucocorticoid therapy for IPF and may be a predictor of IPF treatment outcome.
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http://dx.doi.org/10.1089/gtmb.2015.0057 | DOI Listing |
Science
January 2025
Center for Pulmonary Vascular Biology and Medicine, Pittsburgh, Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA.
Vascular inflammation regulates endothelial pathophenotypes, particularly in pulmonary arterial hypertension (PAH). Dysregulated lysosomal activity and cholesterol metabolism activate pathogenic inflammation, but their relevance to PAH is unclear. Nuclear receptor coactivator 7 () deficiency in endothelium produced an oxysterol and bile acid signature through lysosomal dysregulation, promoting endothelial pathophenotypes.
View Article and Find Full Text PDFPLoS One
January 2025
Cancer Center, Kagoshima University Hospital, Kagoshima, Japan.
Kinase-related gene fusion and point mutations play pivotal roles as drivers in cancer, necessitating optimized, targeted therapy against these alterations. The efficacy of molecularly targeted therapeutics varies depending on the specific alteration, with great success reported for such therapeutics in the treatment of cancer with kinase fusion proteins. However, the involvement of actionable alterations in solid tumors, especially regarding kinase fusions, remains unclear.
View Article and Find Full Text PDFAnnu Rev Pharmacol Toxicol
January 2025
Clinical and Translational Science Institute, Colleges of Medicine and Pharmacy, The Ohio State University, Columbus, Ohio, USA.
Pharmacogenetic variation is common and an established driver of response for many drugs. There has been tremendous progress in pharmacogenetics knowledge over the last 30 years and in clinical implementation of that knowledge over the last 15 years. But there have also been many examples where translation has stalled because of the lack of available data sets for discovery or validation research.
View Article and Find Full Text PDFAnn 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).
Int J Epidemiol
December 2024
International Agency for Research on Cancer (IARC/WHO), Nutrition and Metabolism Branch, Lyon, France.
Background: Adiposity is an established risk factor for colorectal cancer (CRC). The pathways underlying this relationship, and specifically the role of circulating proteins, are unclear.
Methods: Utilizing two-sample univariable Mendelian randomization (UVMR), multivariable Mendelian randomization (MVMR), and colocalization, based on summary data from large sex-combined and sex-specific genetic studies, we estimated the univariable associations between: (i) body mass index (BMI) and waist-hip ratio (WHR) and overall and site-specific (colon, proximal colon, distal colon, and rectal) CRC risk, (ii) BMI and WHR and circulating proteins, and (iii) adiposity-associated circulating proteins and CRC risk.
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