Bajdak-Rusinek Karolina, Fus-Kujawa Agnieszka, Buszman Piotr, Żyła-Uklejewicz Dorota, Jelonek Katarzyna, Musiał-Kulik Monika, Fernandez Carlos, Michalak Magdalena, George Kurian, Kasperczyk Janusz, Buszman Paweł
Department of Medical Genetics, Faculty of Medical Sciences in Katowice, Medical University of Silesia, 40-752 Katowice, Poland.
Cardiology Department, Andrzej Frycz Modrzewski Krakow University, 30-705 Krakow, Poland.
Biomedicines. 2023 Jan 25;11(2):343. doi: 10.3390/biomedicines11020343.
Ischemic heart disease (IHD) is one of the main focuses in today's healthcare due to its implications and complications, and it is predicted to be increasing in prevalence due to the ageing population. Although the conventional pharmacological and interventional methods for the treatment of IHD presents with success in the clinical setting, the long-term complications of cardiac insufficiency are on a continual incline as a result of post-infarction remodeling of the cardiac tissue. The migration and involvement of stem cells to the cardiac muscle, followed by differentiation into cardiac myocytes, has been proven to be the natural process, though at a slow rate. SDF-1α is a novel candidate to mobilize stem cells homing to the ischemic heart. Endogenous SDF-1α levels are elevated after myocardial infarction, but their presence gradually decreases after approximately seven days. Additional administration of SDF-1α-releasing microspheres could be a tool for the extension of the time the stem cells are in the cardiac tissue after myocardial infarction. This, in turn, could constitute a novel therapy for more efficient regeneration of the heart muscle after injury. Through this practical study, it has been shown that the controlled release of SDF-1α from biodegradable microspheres into the pericardial sac fourteen days after myocardial infarction increases the concentration of exogenous SDF-1α, which persists in the tissue much longer than the level of endogenous SDF-1α. In addition, administration of SDF-1α-releasing microspheres increased the expression of the factors potentially involved in the involvement and retention of myocardial stem cells, which constitutes vascular endothelial growth factor A (VEGFA), stem cell factor (SCF), and vascular cell adhesion molecules (VCAMs) at the site of damaged tissue. This exhibits the possibility of combating the basic limitations of cell therapy, including ineffective stem cell implantation and the ability to induce the migration of endogenous stem cells to the ischemic cardiac tissue and promote heart repair.
缺血性心脏病(IHD)因其影响和并发症,是当今医疗保健的主要关注焦点之一,并且预计随着人口老龄化其患病率将不断上升。尽管用于治疗IHD的传统药理学和介入方法在临床环境中取得了成功,但由于心肌梗死后心脏组织的重塑,心脏功能不全的长期并发症仍在持续增加。干细胞迁移并参与到心肌中,随后分化为心肌细胞,这已被证明是自然过程,不过速度较慢。基质细胞衍生因子-1α(SDF-1α)是动员干细胞归巢至缺血心脏的一种新候选物。心肌梗死后内源性SDF-1α水平会升高,但大约七天后其含量会逐渐下降。额外给予释放SDF-1α的微球可能是延长心肌梗死后干细胞在心脏组织中停留时间的一种手段。这反过来可能构成一种新的疗法,用于更有效地促进损伤后心肌的再生。通过这项实际研究表明,在心肌梗死后十四天将可生物降解微球中的SDF-1α控释到心包囊中,可提高外源性SDF-1α的浓度,其在组织中的持续时间比内源性SDF-1α水平长得多。此外,给予释放SDF-1α的微球增加了可能参与心肌干细胞参与和滞留的因子的表达,这些因子在受损组织部位包括血管内皮生长因子A(VEGFA)、干细胞因子(SCF)和血管细胞黏附分子(VCAM)。这显示出对抗细胞治疗基本局限性的可能性,包括无效的干细胞植入以及诱导内源性干细胞迁移至缺血心脏组织并促进心脏修复的能力。