Hurskainen Maria, Ainasoja Olli, Lemström Karl B
Division of Pediatric Cardiology, New Children's Hospital, Helsinki University Hospital and University of Helsinki, 00290 Helsinki, Finland.
Pediatric Research Centre, New Children's Hospital, Helsinki University Hospital and University of Helsinki, 00290 Helsinki, Finland.
J Cardiovasc Dev Dis. 2021 Dec 12;8(12):180. doi: 10.3390/jcdd8120180.
The median survival of patients with heart transplants is relatively limited, implying one of the most relevant questions in the field-how to expand the lifespan of a heart allograft? Despite optimal transplantation conditions, we do not anticipate a rise in long-term patient survival in near future. In order to develop novel strategies for patient monitoring and specific therapies, it is critical to understand the underlying pathological mechanisms at cellular and molecular levels. These events are driven by innate immune response and allorecognition driven inflammation, which controls both tissue damage and repair in a spatiotemporal context. In addition to immune cells, also structural cells of the heart participate in this process. Novel single cell methods have opened new avenues for understanding the dynamics driving the events leading to allograft failure. Here, we review current knowledge on the cellular composition of a normal heart, and cellular mechanisms of ischemia-reperfusion injury (IRI), acute rejection and cardiac allograft vasculopathy (CAV) in the transplanted hearts. We highlight gaps in current knowledge and suggest future directions, in order to improve cellular and molecular understanding of failing heart allografts.
心脏移植患者的中位生存期相对有限，这意味着该领域最相关的问题之一——如何延长心脏同种异体移植物的寿命？尽管移植条件理想，但我们预计近期患者的长期生存率不会提高。为了开发患者监测和特定治疗的新策略，了解细胞和分子水平上的潜在病理机制至关重要。这些事件由先天免疫反应和同种异体识别驱动的炎症所驱动，炎症在时空背景下控制着组织损伤和修复。除免疫细胞外，心脏的结构细胞也参与这一过程。新型单细胞方法为理解导致同种异体移植物失败的事件动态开辟了新途径。在这里，我们综述了关于正常心脏细胞组成以及移植心脏中缺血再灌注损伤（IRI）、急性排斥反应和心脏同种异体血管病变（CAV）的细胞机制的现有知识。我们强调当前知识的空白并提出未来方向，以增进对失败心脏同种异体移植物的细胞和分子理解。
