The aim is to describe the involvement of matrix metalloprotease (MMP), A Disintegrin And Metalloproteases (ADAM), tissue inhibitors of MMP (TIMP) polymorphisms and the role of α-2 Macroglobulin (α-2M) in chronic obstructive pulmonary disease (COPD) development and progression, with a focus on interventions with synthetic MMP inhibitors alone or associated with current drugs used in COPD therapy in order to restore MMPs/TIMPs imbalance.
Overexpression of GLP-1 receptors suppresses proliferation and cytokine release by airway smooth muscle cells of patients with chronic obstructive pulmonary disease via activation of ABCA1.
Modulation of these pathways through manipulation of ABCA1 activity effectively blocks cigarette smoke-induced inflammation and provides a potential novel therapeutic approach for the treatment of chronic obstructive pulmonary disease.-Sonett, J., Goldklang, M., Sklepkiewicz, P., Gerber, A., Trischler, J., Zelonina, T., Westerterp, M., Lemaître, V., Okada, V., D'Armiento, J.
This cross-sectional study aims to develop and validate a cutoff point for FFM depletion based on Brazilian patients with chronic obstructive pulmonary disease (COPD) and to verify its association and of previously published cutoffs with extrapulmonary manifestations.
Impact of ABCB1 single-nucleotide polymorphisms on treatment outcomes with salmeterol/fluticasone combination therapy for stable chronic obstructive pulmonary disease.
This is the first study linking MRP1 SNPs with lung function and inflammatory markers in COPD patients, suggesting a role of MRP1 SNPs in the severity of COPD in addition to their association with MRP1 protein level in bronchial biopsies.
These findings show that Notch1 and MRP1 might have a potential protective effect in the COPD process and become a new therapeutic target for COPD or other lung diseases.
The ATP-binding cassette transporter ABCC1 [i.e. multidrug resistance-associated protein 1 (MRP1)] is a membrane-bound pump excreting a variety of xenobiotics from the cell, and thus ABCC1 may play an important role in smoking-related lung function loss and development of chronic obstructive pulmonary disease (COPD).
Early invasive strategy resulted in lower in-hospital mortality and marginally shorter length of stay but higher hospitalization cost in NSTE-ACS with COPD.
All patients with chronic obstructive pulmonary disease who received angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for more than 90 days between 2000 and 2005 were recruited for this study.
Vitamin D receptor FokI and BsmI genotypes and the (I/D) angiotensin-converting enzyme (ACE) and bradykinin receptor (+9/-9) genotypes were identified in 107 patients with stable COPD [x +/- SD forced expiratory volume in 1 s (FEV(1)): 34.5 +/- 16.5] and 104 healthy, age-matched control subjects.
These findings suggest that the ability of oxygen administration to improve tissue oxygenation during exercise is associated with the ACE genotypes in COPD patients.
We previously showed that the D rather than the I polymorphic variant of the angiotensin-converting enzyme (ACE) gene is associated with preserved quadriceps strength in COPD.
In HHF, the increase in the use of heart failure (HF) medications at hospital discharge was greater in non-COPD than in COPD for angiotensin-converting enzyme inhibitors (+13.7% vs. +7.2%), beta-blockers (+20.6% vs. +11.8%) and mineralocorticoid receptor antagonists (+20.9% vs. +17.3%), thus widening the gap in HF treatment already existing between the two groups at admission.
Our meta-analytical findings demonstrated that the ACE gene I/D polymorphism was not associated with the risk of chronic obstructive pulmonary disease.
The DD genotype of the angiotensin converting enzyme gene is negatively associated with right ventricular hypertrophy in male patients with chronic obstructive pulmonary disease.