Gouty arthritis (GA)
● Symptoms and Causes
Epidemiology, cause and symptoms :Gout is the most common inflammatory arthritis with about 2–4% of prevalence worldwide, mainly in men over 40 and particularly in those with underlying comorbidities such as obesity, hypertension, coronary artery disease, diabetes, or metabolic diseases. The characteristic gouty flare has a distinctive clinical feature, achieving an acute painful synovitis caused by monosodium urate (MSU) crystals deposition in joints.
GA as an Autoimmune disease: MSU triggered the activation of NLRP3, which was the key biomarker in the cycle of GA inflammation. NLRP3 increases the presentation of IL-1β and IL-18,then the neutrophil gathered and degranulation in the joint,which causes the joint inflammation.
Desai J, Steiger S, Anders HJ. Molecular Pathophysiology of Gout. Trends Mol Med. 2017;23(8):756-768. doi:10.1016/j.molmed.2017.06.005
● Models in place 【Date➡Models】
●MSU Induced GA Model in mice 【Mechanism】Monosodium urate (MSU) crystals, the etiological agent of gout, are formed in joints and periarticular tissues due to long-lasting hyperuricemia. MSU crystal-triggered NLRP3 inflammasome activation and interleukin 1β (IL-1β) release are known to have key roles in gouty arthritis, recent studies revealed that MSU crystal-induced necrosis also plays a critical role in this process. |
Gouty arthritis (GA)
● Symptoms and Causes
Epidemiology, cause and symptoms :Gout is the most common inflammatory arthritis with about 2–4% of prevalence worldwide, mainly in men over 40 and particularly in those with underlying comorbidities such as obesity, hypertension, coronary artery disease, diabetes, or metabolic diseases. The characteristic gouty flare has a distinctive clinical feature, achieving an acute painful synovitis caused by monosodium urate (MSU) crystals deposition in joints.
GA as an Autoimmune disease: MSU triggered the activation of NLRP3, which was the key biomarker in the cycle of GA inflammation. NLRP3 increases the presentation of IL-1β and IL-18,then the neutrophil gathered and degranulation in the joint,which causes the joint inflammation.
Desai J, Steiger S, Anders HJ. Molecular Pathophysiology of Gout. Trends Mol Med. 2017;23(8):756-768. doi:10.1016/j.molmed.2017.06.005
● Models in place 【Date➡Models】
●MSU Induced GA Model in mice 【Mechanism】Monosodium urate (MSU) crystals, the etiological agent of gout, are formed in joints and periarticular tissues due to long-lasting hyperuricemia. MSU crystal-triggered NLRP3 inflammasome activation and interleukin 1β (IL-1β) release are known to have key roles in gouty arthritis, recent studies revealed that MSU crystal-induced necrosis also plays a critical role in this process. |