Can estrogens promote hypertension during systemic lupus erythematosus?

Abstract

SLE is a chronic autoimmune inflammatory disorder that predominantly affects young women. Based on this observation, it has been speculated that sex steroids, particularly estrogens, contribute to SLE disease progression. Young women with SLE are at an increased risk for the development of hypertension yet the reasons for this are unclear. One potential mechanism for the increased risk of hypertension during SLE is the chronic inflammation caused by immune complex mediated tissue injury. Estrogens are known to have an immunomodulatory role that can lead to the production of characteristic autoantibodies important for immune complex formation. Therefore, it is conceivable that during SLE estrogens contribute to tissue injury, increased inflammation and hypertension. This brief review discusses the increased risk for hypertension during SLE, the role of estrogens in immune system function, evidence for estrogens in SLE, and a possible link between estrogens and SLE hypertension.

Figure 1

Treatment of a mouse model of SLE with rosiglitazone reduces renal inflammation. (A) Previous work from our laboratory show that macrophage and monocyte infiltration (noted by black arrows) is reduced in the kidneys of the NZBWF1 mouse model of SLE after treatment with rosiglitazone (image taken at 40× magnification) (B) The expression of the chemokine, osteopontin, is reduced in the renal cortex of NZBWF1 mice treated with rosiglitazone. (figures from reference 21)

Figure 2

The NZBWF1 mouse model of SLE develops hypertension. The control used is the NZW/LacJ mouse. Pressure was measured in conscious freely moving mice at 36 weeks of age. (figure from reference 59)