PDF(Pubmed)
Abstract：
Urolithiasis is a high‑incidence disease caused by calcium oxalate (mainly), uric acid, calcium phosphate, struvite, apatite, cystine and other stones. The development of kidney stones is closely related to renal tubule cell damage and crystal adhesion and aggregation. Cell death, comprising the core steps of cell damage, can be classified into various types (i.e., apoptosis, ferroptosis, necroptosis and pyroptosis). Different crystal types, concentrations, morphologies and sizes cause tubular cell damage via the regulation of different forms of cell death. Oxidative stress caused by high oxalate or crystal concentrations is considered to be a precursor to a variety of types of cell death. In addition, complex crosstalk exists among numerous signaling pathways and their key molecules in various types of cell death. Urolithiasis is considered a metabolic disorder, and tricarboxylic acid cycle‑related molecules, such as citrate and succinate, are closely related to cell death and the inhibition of stone development. However, a literature review of the associations between kidney stone development, metabolism and various types of cell death is currently lacking, at least to the best of our knowledge. Thus, the present review summarizes the major advances in the understanding of regulated cell death and urolithiasis progression.
摘要：
尿石症是由草酸钙（主要）引起的高发疾病，尿酸,磷酸钙,鸟粪石,磷灰石,胱氨酸和其他结石。肾结石的发生发展与肾小管细胞损伤和晶体粘附聚集密切相关。细胞死亡,包括细胞损伤的核心步骤，可以分为各种类型(即，凋亡，铁性凋亡,坏死和焦亡）。不同的晶体类型，浓度,形态和大小通过调节不同形式的细胞死亡引起肾小管细胞损伤。由高草酸盐或晶体浓度引起的氧化应激被认为是各种类型的细胞死亡的前兆。此外,在各种类型的细胞死亡中，许多信号通路及其关键分子之间存在复杂的串扰。尿石症被认为是一种代谢紊乱,和三羧酸循环相关分子，如柠檬酸盐和琥珀酸盐，与细胞死亡和结石发育抑制密切相关。然而,肾结石发展之间的关联的文献综述，目前缺乏新陈代谢和各种类型的细胞死亡，至少就我们所知.因此，本综述总结了在了解调节细胞死亡和尿石症进展方面的主要进展。
