Wang X L, Liu S X, Wilcken D E
Department of Cardiovascular Medicine, University of New South Wales, Prince Henry/Prince of Wales Hospitals, Sydney, Australia.
Cardiovasc Res. 1997 May;34(2):404-10. doi: 10.1016/s0008-6363(97)00033-3.
Transforming growth factor beta 1 (TGF-beta 1), a multifunctional cytokine, is involved in many physiological and pathological processes and possibly in atherogenesis.
We explored the association between circulating plasma TGF-beta 1 measured by ELISA and coronary artery disease (CAD) assessed angiographically in 371 Caucasian patients (269 men and 102 women) aged < or = 65 years.
While mean +/- s.e.m total TGF-beta 1 was not different among patients with (56.9 +/- 1.5 ng/ml) or without (54.6 +/- 2.8 ng/ml) angiographically demonstrable CAD, naturally active TGF-beta 1 was significantly higher in CAD patients (1.74 +/- 0.18 vs 0.96 +/- 0.17 ng/ml, P < 0.01). Active TGF-beta 1 increased with the number of major coronary arteries with more than 50% luminal obstruction (P < 0.01) and patients with triple vessel disease had twice the level of those with no or mild vessel disease (2.15 +/- 0.46 vs 1.12 +/- 0.14 ng/ml, P < 0.001). We found no relationship between TGF-beta 1 and Lp(a), but TGF-beta 1 was significantly correlated with circulating fibrinogen (r = 0.178, P = 0.005) and fasting glucose (r = 0.177, P = 0.007) levels.
Our study identifies an increase in active TGF-beta 1 levels with both the occurrence and severity of CAD which is independent of standard CAD risk factors. This may reflect a 'double-edged sword' effect of TGF-beta 1 in that it may reduce atherogenesis by inhibiting smooth muscle cell proliferation but, when there is ongoing vessel wall injury, enhance it by promoting excessive extracellular matrix accumulation. The outcome could represent a complex balance between these two competing influences.
转化生长因子β1（TGF-β1）是一种多功能细胞因子，参与许多生理和病理过程，可能也参与动脉粥样硬化的发生。
我们在371名年龄≤65岁的白种人患者（269名男性和102名女性）中，探讨了通过酶联免疫吸附测定法（ELISA）检测的循环血浆TGF-β1与通过血管造影评估的冠状动脉疾病（CAD）之间的关联。
血管造影显示有CAD的患者（56.9±1.5 ng/ml）和无CAD的患者（54.6±2.8 ng/ml）之间，总的TGF-β1均值±标准误没有差异，但天然活性TGF-β1在CAD患者中显著更高（1.74±0.18 vs 0.96±0.17 ng/ml，P<0.01）。活性TGF-β1随着管腔阻塞超过50%的主要冠状动脉数量增加而升高（P<0.01），三支血管病变患者的水平是无血管病变或轻度血管病变患者的两倍（2.15±0.46 vs 1.12±0.14 ng/ml，P<0.001）。我们发现TGF-β1与脂蛋白（a）[Lp（a）]之间没有关系，但TGF-β1与循环纤维蛋白原（r = 0.178，P = 0.005）和空腹血糖（r = 0.177，P = 0.007）水平显著相关。
我们的研究发现活性TGF-β1水平随着CAD的发生和严重程度增加，且独立于标准的CAD危险因素。这可能反映了TGF-β1的“双刃剑”效应，即它可能通过抑制平滑肌细胞增殖来减少动脉粥样硬化的发生，但在血管壁持续损伤时，通过促进细胞外基质过度积聚来增强动脉粥样硬化。结果可能代表了这两种相互竞争影响之间的复杂平衡。
