Matucci-Cerinic Marco, Manetti Mirko, Bruni Cosimo, Chora Ines, Bellando-Randone Silvia, Lepri Gemma, De Paulis Amato, Guiducci Serena
Department of Experimental and Clinical Medicine, Division of Rheumatology and Scleroderma Unit, Azienda Ospedaliera Universitaria Careggi, University of Florence, Viale Pieraccini 18, 50139, Florence, Italy.
Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134, Florence, Italy.
Arthritis Res Ther. 2017 Jul 6;19(1):162. doi: 10.1186/s13075-017-1370-5.
Systemic sclerosis is considered a disease dominated by a "loss of angiogenesis", although in its early phases evidence indicates a disturbed angiogenic response only. In fact, microvascular changes are primarily due to endothelial cell injury, triggering downstream significant enlargement of the capillary in an inflammatory environment, followed by capillary rupture (microhemorrhages). Subsequent pro-angiogenic efforts lead to an aberrant angiogenesis and, eventually, to a total loss of vessel repair and regeneration (loss of angiogenesis). This clearly suggests that the pathogenetic process has a steady progression: from an early excessive pro-angiogenesis, to an aberrant microvascular regeneration, then ending with a late loss of angiogenesis. Herein, we suggest the loss of angiogenesis should not be considered as an overall "myth" characterizing systemic sclerosis but as a very late event of the vascular pathogenesis. Future research should be oriented essentially on the earlier phases dominated by excessive pro-angiogenesis and microvascular aberration.
系统性硬化症被认为是一种以“血管生成丧失”为主导的疾病,尽管在其早期阶段,证据仅表明血管生成反应紊乱。事实上,微血管变化主要是由于内皮细胞损伤,在炎症环境中引发下游毛细血管显著扩张,随后毛细血管破裂(微出血)。随后的促血管生成努力导致异常血管生成,并最终导致血管修复和再生完全丧失(血管生成丧失)。这清楚地表明,发病过程有一个稳定的进展:从早期过度的促血管生成,到异常的微血管再生,最后以晚期血管生成丧失告终。在此,我们认为血管生成丧失不应被视为系统性硬化症的整体“虚构特征”,而应被视为血管发病机制中非常晚期的事件。未来的研究应主要针对以过度促血管生成和微血管异常为主导的早期阶段。