Rheumatoid arthritis (RA) is a chronic, invasive autoimmune disease that can cause joint deformity, even complete loss of joint function. This autoimmune disease has a high disability rate, poor prognosis, and is prone to repeated attacks, so it is often referred to as “deathless cancer”. Furthermore, the RA treatment cycle is very long, so it will bring a heavy economic burden to patients' families and society.
Recently, it’s suggested that characteristics of RA are excessive synovial tissue hyperplasia, pannus formation, and erosion of cartilage. Importantly, the excessive proliferation of fibroblast-like synoviocytes (FLS) is generally recognized as the pathological basis of RA. The activated FLS can secrete various cytokines, chemokines, and metalloproteinases (MMPs) to induce inflammation, angiogenesis, cartilage destruction, and joint injury. Consequently, FLS plays key immunomodulatory roles in the development of RA.
Herein, we propose to provide an academic platform for the topic of “Immunomodulatory Roles of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis”. This Research Topic aims to collect outstanding scientific papers to uncover the immunomodulatory roles, functions, and mechanisms of FLS in the development of RA, as well as to explore the possible molecular targets and intervention ways for treating RA involved in FLS.
We welcome the submission of Original Research and Review articles that explore the potential topics, including but not limited to the following:
(1) Immunomodulatory roles and functions of FLS in the development of RA.
(2) Novel molecular mechanisms and signal transduction pathways related to FLS involved in the development of RA.
(3) Novel strategies targeting FLS to intervene RA, such as induction of apoptosis, autophagy & ferroptosis, intestinal microflora regulation, etc.
(4) Novel molecular targets related to FLS for the treatment of RA and its potential agonists/inhibitors.
(5) Other topics related to the relationship between FLS and RA are also welcome.
Rheumatoid arthritis (RA) is a chronic, invasive autoimmune disease that can cause joint deformity, even complete loss of joint function. This autoimmune disease has a high disability rate, poor prognosis, and is prone to repeated attacks, so it is often referred to as “deathless cancer”. Furthermore, the RA treatment cycle is very long, so it will bring a heavy economic burden to patients' families and society.
Recently, it’s suggested that characteristics of RA are excessive synovial tissue hyperplasia, pannus formation, and erosion of cartilage. Importantly, the excessive proliferation of fibroblast-like synoviocytes (FLS) is generally recognized as the pathological basis of RA. The activated FLS can secrete various cytokines, chemokines, and metalloproteinases (MMPs) to induce inflammation, angiogenesis, cartilage destruction, and joint injury. Consequently, FLS plays key immunomodulatory roles in the development of RA.
Herein, we propose to provide an academic platform for the topic of “Immunomodulatory Roles of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis”. This Research Topic aims to collect outstanding scientific papers to uncover the immunomodulatory roles, functions, and mechanisms of FLS in the development of RA, as well as to explore the possible molecular targets and intervention ways for treating RA involved in FLS.
We welcome the submission of Original Research and Review articles that explore the potential topics, including but not limited to the following:
(1) Immunomodulatory roles and functions of FLS in the development of RA.
(2) Novel molecular mechanisms and signal transduction pathways related to FLS involved in the development of RA.
(3) Novel strategies targeting FLS to intervene RA, such as induction of apoptosis, autophagy & ferroptosis, intestinal microflora regulation, etc.
(4) Novel molecular targets related to FLS for the treatment of RA and its potential agonists/inhibitors.
(5) Other topics related to the relationship between FLS and RA are also welcome.
