Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Juiz de Fora, Rua José Lourenço Khelmer - s/n, Campus Universitário, São Pedro, Juiz de Fora, Minas Gerais, 36036900, Brazil.
Departamento de Biofísica e Biometria, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Boulevard Vinte e Oito de Setembro, 87, fundos, Vila Isabel, Rio de Janeiro, 20551030, Brazil.
Lasers Med Sci. 2024 Nov 1;39(1):267. doi: 10.1007/s10103-024-04218-5.
Photodynamic therapy (PDT) is an alternative to cancer treatment, demonstrating selectivity and significant cytotoxicity on malignant tissues. Such therapy involves two nontoxic components: photosensitizer (PS) and non-ionizing radiation. In optimal dosage combinations, PDT causes cellular and tissue effects by oxygen-dependent processes, leading tumor cells to regulated cell death pathways. Regulated necrosis, called necroptosis, can be triggered by PDT and is characterized by caspase-8 inhibition and RIPK1, RIPK3, and MLKL activities, leading to plasma membrane pores formation with subsequent cellular content release into the extracellular space. For this review, studies accessed by PubMed describing the relation between necroptosis and PDT were summarized. The results showed that PDT can trigger necroptosis mechanisms in different tumor cells. Moreover, a mix of different cell death types can co-occur. It is also important to highlight that necroptosis triggered by PDT is related to damage-associated molecular patterns (DAMPs) release, involving immunogenic cell death and vaccination. The cell death response is directly related to the photosensitizer chemical characteristics, concentration, incubation time, cellular location, and irradiation parameters. The synergism among all cell death types is an excellent advantage for avowing tumor resistance mechanisms and developing new solutions.
光动力疗法（PDT）是癌症治疗的一种替代方法，对恶性组织具有选择性和显著的细胞毒性。这种疗法涉及两种无毒成分：光敏剂（PS）和非电离辐射。在最佳剂量组合下，PDT 通过氧依赖性过程引起细胞和组织效应，导致肿瘤细胞发生受调控的细胞死亡途径。受调控的坏死，称为坏死性凋亡，可以被 PDT 触发，其特征是半胱天冬酶-8 抑制和 RIPK1、RIPK3 和 MLKL 活性，导致质膜孔形成，随后细胞内容物释放到细胞外空间。本文综述了通过 PubMed 检索到的描述坏死性凋亡与 PDT 之间关系的研究。结果表明，PDT 可以在不同的肿瘤细胞中触发坏死性凋亡机制。此外，不同类型的细胞死亡可以同时发生。同样重要的是要强调，PDT 触发的坏死性凋亡与损伤相关分子模式（DAMPs）的释放有关，涉及免疫原性细胞死亡和疫苗接种。细胞死亡反应与光敏剂的化学特性、浓度、孵育时间、细胞位置和辐射参数直接相关。所有细胞死亡类型的协同作用是克服肿瘤耐药机制和开发新解决方案的绝佳优势。
