Endothelial Function and its Implications for Cardiovascular and Renal Disease in Systemic Lupus Erythematosus

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Profile of adiponectin in health and disease

Adiponectin (also known as 30-kd adipocyte complement-related protein [Acrp30]) is a secreted protein that is constitutively produced by adipocytes. Adiponectin, a trimer in serum, is a 30-kd protein consisting of four domains, including signal peptide at the N-terminus, a variable domain, a collagenous domain, and a C-terminal globular domain homologous to C1q. The protein is well characterized regarding its capacity to improve insulin sensitivity. During the early 1990s the best-characterized

Membrane endothelial protein C receptor: protection of the endothelium

EPCR, which has been cloned in mice and human tissues,26 is constitutively expressed by endothelial cells, particularly in large blood vessels and monocyte/macrophages. EPCR is a 46-kd type 1 transmembrane glycoprotein with structural features consistent with an antigen-presenting groove analogous to major histocompatibility complex (MHC) class 1 and the CD1 family of proteins. Its structure consists of a large extracellular domain (221 amino acids), a transmembrane domain (25 amino acids), and

Endothelial dysfunction and progression of atherosclerosis and renal disease

The usefulness of biomarkers, which identify patients who have endothelial dysfunction and progression of atherosclerosis and renal disease, has fallen short of the mark. This section reviews the biomarker discovery initiative in the context of inflammation hypothesis and Schwartzman phenomenon. Recent studies are then reviewed that offer a new direction for risk stratification. New mechanistic insights into the pathophysiology underlying accelerated atherogenesis and renal disease are then

Summary

Prior conceptual framework portrayed widespread endothelial activation in the context of the Schwartzman phenomenon. The focus was solely restricted to analysis of proinflammatory molecules. Findings suggested that the anti-injury molecules (eg, adiponectin, mEPCR) might be down-regulated. In fact, the authors' early hypothesis was that adiponectin might be lower in patients who have plaque, and mEPCR is lower in progressive nephritis. The fact that the opposite was observed challenges the

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  • Cited by (6)

    • Inclusion of renal vascular lesions in the 2003 ISN/RPS system for classifying lupus nephritis improves renal outcome predictions

      2013, Kidney International
      Citation Excerpt :

      With regard to premature cardiovascular diseases, some investigators noted that the most common cause of death in patients with lupus of longer disease duration could be attributed to atherosclerosis.26 Risk factors in these patients included longer duration of disease and lower likelihood of treatment with prednisone, cyclophosphamide, or hydroxychloroquine,27 as well other nontraditional factors such as interferon-alpha,28 adiponectin, membrane endothelial protein C receptor,29 complement activation,30 etc. Therefore, appropriate assessment of the extent of atherosclerosis, its association with long-term cardiovascular events, and potential intervention need further studies.

    • Mechanisms of Acute Inflammation and Vascular Injury in SLE

      2013, Dubois' Lupus Erythematosus and Related Syndromes: Eighth Edition
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