2014
DOI: 10.1097/01.mnh.0000444812.65002.cb
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Diverse vascular lesions in systemic lupus erythematosus and clinical implications

Abstract: Vascular lesions in SLE are mediated by a complex interaction between the immune system and other contributing factors. Different therapies developed for vascular lesions, both immunosuppressive and nonimmunosuppressive, should be selected based on the different clinical and pathological characteristics, and our future understanding of the different mechanisms involved.

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Cited by 11 publications
(8 citation statements)
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“…In our study, we found that the probability of SLE patients complicated with serositis was significantly increased if the duration of medicine maintenance therapy less than 1 year. The systemic damage of SLE was induce by vasculitis and non-inflammatory vascular remodeling [38][39][40]. Vasculitis is significantly correlated with the activity of SLE [38], while the pathophysiological mechanisms of noninflammatory vascular remodeling may play an important role when the course of the disease is longer [38,40], which might act as a key factor in the choice of treatment strategy and the prognosis.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In our study, we found that the probability of SLE patients complicated with serositis was significantly increased if the duration of medicine maintenance therapy less than 1 year. The systemic damage of SLE was induce by vasculitis and non-inflammatory vascular remodeling [38][39][40]. Vasculitis is significantly correlated with the activity of SLE [38], while the pathophysiological mechanisms of noninflammatory vascular remodeling may play an important role when the course of the disease is longer [38,40], which might act as a key factor in the choice of treatment strategy and the prognosis.…”
Section: Discussionmentioning
confidence: 99%
“…The systemic damage of SLE was induce by vasculitis and non-inflammatory vascular remodeling [38][39][40]. Vasculitis is significantly correlated with the activity of SLE [38], while the pathophysiological mechanisms of noninflammatory vascular remodeling may play an important role when the course of the disease is longer [38,40], which might act as a key factor in the choice of treatment strategy and the prognosis. Vascular remodeling erodes multiple organs throughout the body along the course of the disease, and they tend to become chronic, requiring long-term drug control or even lifelong medication.…”
Section: Discussionmentioning
confidence: 99%
“…Treatment with coptisine significantly alleviated the impairment of the vascular relaxation response to the endothelium-dependent vasodilator ACh in SLE mice, which suggests that coptisine may prevent vascular endothelial dysfunction. The mechanisms of endothelial dysfunction in SLE patients may be upregulated expression of ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1), increased secretion of chemokines such as MCP-1, IL-6, IL-17A, and TNF-a, and the promotion of the activation of the transcription factor NF-kB p65 in human endothelial cells by immune complexes (Goḿez-Guzmań et al, 2014;Tan et al, 2014). In this study, we found that coptisine significantly alleviated the overexpression of ICAM-1 and IL-17A in the serum.…”
Section: A B Cmentioning
confidence: 99%
“…Therefore, it is still controversial whether renal vascular complications should be considered independent renal prognostic factors for SLE. A series of studies indicated that renal vascular complications are closely associated with clinical disease, disease activity, and renal outcomes, and that renal thrombotic microangiopathy (TMA) is an independent risk factor for the renal prognosis of patients with long-term LN [34,[38][39][40][41].…”
Section: Vascular Lesionsmentioning
confidence: 99%