Ignite Creation Date:
2024-10-25 @ 7:52 PM
Last Modification Date:
2024-10-26 @ 3:35 PM
Study NCT ID:
NCT06503315
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2024-07-10
Brief Title:
Genetic Polymorphism in Matrix Metalloproteinase 9 in Chronic Obstructive Pulmonary Disease in Sohag University Hospital
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Genetic Polymorphism in Matrix Metalloproteinase 9 in Chronic Obstructive Pulmonary Disease in Sohag University Hospital
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Chronic obstructive pulmonary disease COPD is a heterogeneous and complex disease with multiple clinical presentations or phenotypes and remains a highly prevalent condition causing significant morbidity and mortality worldwide
Chronic obstructive pulmonary disease COPD is the third most common cause of global mortality affecting over 210 million individuals
Chronic obstructive pulmonary disease COPD is a chronic airway disease involving chronic local and systemic inflammatory changes clinically characterized by continuous and progressive airflow obstruction with airway remodeling and lung parenchyma destruction as pathological basis
The precise molecular mechanism underlying the pathogenesis of COPD remains unclear Zhang J et al 2021 At present it is generally believed that several risk factors are directly related to the pathogenesis of COPD including host and environmental factors
Among environmental factors smoking exposure to chemicals indoor and outdoor air pollution are risk factors for COPD
Host factors of COPD include antitrypsin-1 excessive deposition of extracellular matrix ECM corticosteroids inflammatory stimuli and metabolic imbalances
Matrix metalloproteinases MMPs is a family of calcium- and zinc-dependent proteinase There are currently at least 26 subtypes that can degrade almost all extracellular matrix and basement membrane components
The MMP-9 gene is located on human chromosome 16 including 13 exons and 12 introns and its regulation mainly occurs at the transcriptional level In the pathogenesis of COPD MMP-9 mainly degrades the extracellular matrix and basement membrane of alveolar wall destroying the normal structure of lung tissue At the same time MMP-9 also repairs the extracellular matrix and participates in respiratory tract reconstruction
In addition MMP-9 can also participate in inflammatory response causing inflammatory cells to accumulate in the airway thus increasing airway responsiveness Study found that MMP-9 is highly expressed in the lung tissues of COPD patients and leads to generation of sputum MMPs are important in COPD They degrade matrix proteins elastin collagen during the disease progression
Therefore the analysis of MMP-9 gene polymorphism is an important starting point to explore the susceptibility to COPD It has been found that there is a mutation from C to T at site 1562 of promoter MMP-9 which may affect the expression level of MMP-9 gene The MMP-9-C1562T polymorphism is an important reason for the abnormal increase of MMP-9 expression level
Chronic obstructive pulmonary disease COPD is the third most common cause of global mortality affecting over 210 million individuals
Chronic obstructive pulmonary disease COPD is a chronic airway disease involving chronic local and systemic inflammatory changes clinically characterized by continuous and progressive airflow obstruction with airway remodeling and lung parenchyma destruction as pathological basis
The precise molecular mechanism underlying the pathogenesis of COPD remains unclear Zhang J et al 2021 At present it is generally believed that several risk factors are directly related to the pathogenesis of COPD including host and environmental factors
Among environmental factors smoking exposure to chemicals indoor and outdoor air pollution are risk factors for COPD
Host factors of COPD include antitrypsin-1 excessive deposition of extracellular matrix ECM corticosteroids inflammatory stimuli and metabolic imbalances
Matrix metalloproteinases MMPs is a family of calcium- and zinc-dependent proteinase There are currently at least 26 subtypes that can degrade almost all extracellular matrix and basement membrane components
The MMP-9 gene is located on human chromosome 16 including 13 exons and 12 introns and its regulation mainly occurs at the transcriptional level In the pathogenesis of COPD MMP-9 mainly degrades the extracellular matrix and basement membrane of alveolar wall destroying the normal structure of lung tissue At the same time MMP-9 also repairs the extracellular matrix and participates in respiratory tract reconstruction
In addition MMP-9 can also participate in inflammatory response causing inflammatory cells to accumulate in the airway thus increasing airway responsiveness Study found that MMP-9 is highly expressed in the lung tissues of COPD patients and leads to generation of sputum MMPs are important in COPD They degrade matrix proteins elastin collagen during the disease progression
Therefore the analysis of MMP-9 gene polymorphism is an important starting point to explore the susceptibility to COPD It has been found that there is a mutation from C to T at site 1562 of promoter MMP-9 which may affect the expression level of MMP-9 gene The MMP-9-C1562T polymorphism is an important reason for the abnormal increase of MMP-9 expression level
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None