Asset Details
Do you wish to reserve the book?
The dual role of thrombospondin-1 in inflammatory regulation during acute respiratory distress syndrome: a mini-review
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The dual role of thrombospondin-1 in inflammatory regulation during acute respiratory distress syndrome: a mini-review
Do you wish to request the book?
The dual role of thrombospondin-1 in inflammatory regulation during acute respiratory distress syndrome: a mini-review
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The dual role of thrombospondin-1 in inflammatory regulation during acute respiratory distress syndrome: a mini-review
2025
Overview
Inflammation serves as a fundamental defense against tissue injury and infection, yet dysregulation can lead to pathological outcomes. Thrombospondin-1 (Thbs1/TSP1), a multifunctional glycoprotein significantly upregulated during inflammation, exemplifies a dualistic regulator with context-dependent roles. Through modulation of cytokine networks and inflammatory cell activity (notably macrophages), Thbs1 critically governs inflammatory responses. Acute respiratory distress syndrome (ARDS), a life-threatening condition fueled by systemic inflammation secondary to infection or trauma, presents complex pathophysiology requiring elucidation. COVID-19 research highlights elevated Thbs1 expression in severe patients, where it demonstrates protective effects against pulmonary damage primarily via extracellular matrix protection, inhibition of neutrophil serine proteases, and TGF-β-dependent repair pathways. However, paradoxical evidence indicates that dysregulated Thbs1 can also contribute to ARDS pathogenesis, potentially by amplifying inflammation, promoting thromboinflammation, or driving fibrosis. Mechanistic insights reveal Thbs1’s influence on ARDS progression through ECM remodeling, serine protease inhibition, and TGF-β activation. While significant progress has been made in understanding Thbs1 signaling, the precise mechanisms dictating its context-dependent switch between protective and pathogenic functions in inflammatory pathways remain a critical area for future investigation.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Animals
/ ARDS
/ COVID-19
/ Disease
/ Fibrosis
/ Generative artificial intelligence
/ Humans
/ Obesity
/ Patients
/ Proteins
/ Respiratory distress syndrome
/ Respiratory Distress Syndrome - immunology
/ Respiratory Distress Syndrome - metabolism
/ Respiratory Distress Syndrome - pathology
/ Thrombospondin 1 - immunology
/ Thrombospondin 1 - metabolism
/ Transforming growth factor-b
/ Writing
