Ignite Creation Date:
2024-10-26 @ 3:39 PM
Last Modification Date:
2024-10-26 @ 3:39 PM
Study NCT ID:
NCT06584643
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2023-12-18
Brief Title:
Evaluation of Serum Gasdermin D Level As a Potential Biomarker of Disease Activity in Vitiligo Patients
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Evaluation of Serum Gasdermin D Level As a Potential Biomarker of Disease Activity in Vitiligo Patients
Status:
NOT_YET_RECRUITING
Status Verified Date:
2023-11
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:
Assessment the serum level of Gasdermin D level in vitiligo patients Correlate its level with disease activity scores using Vitiligo Area Severity Index VASI and Vitiligo Disease Activity VIDA scores and with different disease parameters
Detailed Description:
Vitiligo a common depigmenting skin disorder has an estimated prevalence of 05-2 of the population worldwide The disease is characterized by the selective loss of melanocytes which results in typical nonscaly chalky-white macules In recent years considerable progress has been made in our understanding of the pathogenesis of vitiligo which is now clearly classified as an autoimmune disease
The destruction of melanocyte is thought to be of multifactorial causation Genome-wide associated studies have identified single-nucleotide polymorphisms in a panel of susceptible loci as risk factors in melanocyte death But vitiligo onset cant be solely attributed to a susceptive genetic background
Oxidative stress triggered by elevated levels of reactive oxygen species accounts for melanocytic molecular and organelle dysfunction in addition to the self-responsive immune function directly contributes to the bulk of melanocyte deaths in vitiligo
Moreover apoptosis is the most extensively documented way of melanocyte demise with few melanocytes undergo necrosis But forms of cell death are not merely restricted to apoptosis and necrosis Cells may die from accidental cell death ACD or regulated cell death RCD ACD like necrosis is biologically uncontrolled whereas RCD apoptosis necroptosis pyroptosis oxeiptosis ferroptosis parthanatos etc involves precise signaling cascade and molecular mechanisms
Pyroptosis is mechanistically distinct from other forms of cell death with gasdermin D GSDMD and caspase-14511 activation as its defining feature Upon being stimulated by damage-associated molecular patterns molecules DAMPs pathogen-associated molecular patterns molecules or altered homeostasis caspases are activated to cleave the downstream GSDMD GSDMD fragment with membrane pore-forming activity yields plasma membrane rupture cytosolic content release and concurrent cell swelling and lysis
Gasdermins belong to the pore-forming protein family and consist of six gasdermin proteins including gasdermins A-E The members of the gasdermin family have two domains an N-terminal domain and a C-terminal domain linked by a flexible peptide Upon activation the cleaved N-terminal domain is responsible for inducing pyroptosis GSDMD the most extensively studied executive pyroptosis-executing protein with the clearest mechanism
In a previous study scRNA-seq datasets of skin-derived cells from healthy donors and patients with vitiligo were analysed Results demonstrated that CASP1 CASP4 CASP6 CASP8 and GSDMD expression was significantly upregulated in melanocytes of patients with vitiligo These results indicated that pyroptosis signaling is an important pathway in the development of vitiligo
To the best of our knowledge no previous studies have evaluated the serum level of Gasdermin D as a potential biomarker in vitiligo patients
The destruction of melanocyte is thought to be of multifactorial causation Genome-wide associated studies have identified single-nucleotide polymorphisms in a panel of susceptible loci as risk factors in melanocyte death But vitiligo onset cant be solely attributed to a susceptive genetic background
Oxidative stress triggered by elevated levels of reactive oxygen species accounts for melanocytic molecular and organelle dysfunction in addition to the self-responsive immune function directly contributes to the bulk of melanocyte deaths in vitiligo
Moreover apoptosis is the most extensively documented way of melanocyte demise with few melanocytes undergo necrosis But forms of cell death are not merely restricted to apoptosis and necrosis Cells may die from accidental cell death ACD or regulated cell death RCD ACD like necrosis is biologically uncontrolled whereas RCD apoptosis necroptosis pyroptosis oxeiptosis ferroptosis parthanatos etc involves precise signaling cascade and molecular mechanisms
Pyroptosis is mechanistically distinct from other forms of cell death with gasdermin D GSDMD and caspase-14511 activation as its defining feature Upon being stimulated by damage-associated molecular patterns molecules DAMPs pathogen-associated molecular patterns molecules or altered homeostasis caspases are activated to cleave the downstream GSDMD GSDMD fragment with membrane pore-forming activity yields plasma membrane rupture cytosolic content release and concurrent cell swelling and lysis
Gasdermins belong to the pore-forming protein family and consist of six gasdermin proteins including gasdermins A-E The members of the gasdermin family have two domains an N-terminal domain and a C-terminal domain linked by a flexible peptide Upon activation the cleaved N-terminal domain is responsible for inducing pyroptosis GSDMD the most extensively studied executive pyroptosis-executing protein with the clearest mechanism
In a previous study scRNA-seq datasets of skin-derived cells from healthy donors and patients with vitiligo were analysed Results demonstrated that CASP1 CASP4 CASP6 CASP8 and GSDMD expression was significantly upregulated in melanocytes of patients with vitiligo These results indicated that pyroptosis signaling is an important pathway in the development of vitiligo
To the best of our knowledge no previous studies have evaluated the serum level of Gasdermin D as a potential biomarker in vitiligo patients
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