Serum salusin-α levels in systemic lupus erythematosus and systemic sclerosis

Abstract

Objective: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), chronic inflammatory diseases, demonstrate an increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. Salusin-α is a novel bioactive peptide that suppresses the formation of macrophage foam cells, and its serum level is significantly lower in patients with angiographically proven coronary artery disease. The aims of the study were to assess serum salusin-α level and its potential association with the predictors of atherosclerosis in SLE and SSc. Material and Methods:The study included 20 SLE and 22 SSc patients and 23 healthy controls (HC). All of the participants were female. Tumour necrosis factor-α (TNF-α), IL-6 and salusin-α levels, homeostasis model assessment for insulin resistance (HOMA-IR) index and common carotid intima-media thickness (IMT) were determined.Results: Salusin-α levels were lower and the IMTs were higher in the SLE and SSc groups than in the HC group. The salusin-α level was correlated with neither the disease activity scores nor cytokine levels and IMT in the SLE and SSc groups, although it was correlated with triglyceride level in the SLE group (r=-0.564, p=0.012), and with HOMA-IR index in the HC group (r=0.485, p=0.019). Conclusion:The present preliminary study may support the idea that SSc leads to subclinical atherosclerosis, as in SLE. Moreover, it can be concluded that the decreased salusin-α levels in SLE and SSc may contribute to subclinical atherosclerosis. However, further studies with larger sample size are needed to demonstrate this contribution in SLE and SSc.

Overexpression of Salusin-α Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model

“…Importantly, we found that overexpression of the salusin- α gene decreased the intima thickness in rabbits. Intimal hyperplasia in atherosclerotic rabbit models is usually caused by excessive accumulation of intracellular lipids by intimal cells [ 27 – 29 ], and the salusin- α gene has been reported to reduce hypertension and inhibited macrophage foam [ 14 , 15 ]. Thus, the finding that overexpression of salusin- α decreased intimal thickness could be related to inhibition of the proliferation of vascular endothelial cells.…”

“…In addition, this protein is also involved in the prevention of macrophage foam cell formation by downregulating acetyl-coenzyme A acetyltransferase 1 (ACAT1), thereby affecting atherosclerosis [ 10 , 12 , 13 ]. Some reports have shown the negative correlation between salusin- α levels in serum and the degree of vascular stenosis, suggesting that salusin- α may have applications as a diagnostic reference in atherosclerotic disease [ 14 , 15 ]. However, the mechanisms through which salusin- α regulates atherosclerosis in vivo are unclear.…”

Serum interleukin-6 level is correlated with the disease activity of systemic lupus erythematosus: a meta-analysis

“…The serum IL-6 levels ranged from 4.272±0.4222 to 123.71±81.783 (pg/mL) in SLE patients and 0.93 ± 0.95 to 10.46 ± 4.33 (pg/mL) in healthy controls. A total of 13 studies compared the serum IL-6 levels between SLE patients and healthy controls (23)(24)(25)(27)(28)(29)(32)(33)(34)39,40,43,46). Serum IL-6 levels between active and inactive SLE patients were compared in 9 studies (24)(25)(26)29,31,39,(41)(42)(43).…”

Implant-Supported Prosthetic Treatment in a Patient with Systemic Sclerosis: Case Report

“…9 Arnett ve ark., yaptıkları çalışmada, birinci derece yakınlarında SSk bulunan bireylerde, SSk gelişme olasılığının arttığını, normal populasyonda SSk gelişme riski %0,026 iken, birinci derece yakınlarında SSk bulunan bireylerde bu riskin %2,6 olduğunu belirtmişlerdir. 37 Nietert ve Silver, çevresel ve mesleksel faktörlerin SSk etiyolojisindeki yerini incelemiş ve bu faktörlerin tek başına SSk etiyopatogenezinde etkili olamayacağını bildirmişlerdir.…”

“…2,8 SSk'nın etiyolojisi tam olarak açıklanamamasına karşın çevresel faktörler, geçirilmiş enfeksiyonlar, mikrokimerizm ve genetik yatkınlık, patojenik sü-reci tetikleyen olası aracılar olarak gösterilmektedir. 9 SSk patogenezinin vaskülopati, immün aktivasyon ve fibroz triadı ile karakterize olduğu kabul edilmektedir. [10][11][12] Mikrovaskülopatinin kapillereskopi ile teşhis edilmesi SSk'nın erken tanısı için önemlidir.…”