In the last decade, the role of apoptosis in the pathophysiology of acute kidney injury (AKI) and AKI to chronic kidney disease (CKD) progression has been revisited as our understanding of ferroptosis and necroptosis has emerged. A growing body of evidence, reviewed here, ascribes a central pathophysiological role for ferroptosis and necroptosis to AKI, nephron loss, and acute tubular necrosis. We will introduce concepts to the non-cell-autonomous manner of kidney tubular injury during ferroptosis, a phenomenon that we refer to as a "wave of death." We hypothesize that necroptosis might initiate cell death propagation through ferroptosis. The remaining necrotic debris requires effective removal processes to prevent a secondary inflammatory response, referred to as necroinflammation. Open questions include the differences in the immunogenicity of ferroptosis and necroptosis, and the specificity of necrostatins and ferrostatins to therapeutically target these processes to prevent AKI-to-CKD progression and end-stage renal disease.

中文翻译：

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肾脏的肥大病和坏死病。

在过去的十年中，随着我们对肥大病和坏死性病的认识逐渐显现，细胞凋亡在急性肾损伤（AKI）和AKI向慢性肾脏病（CKD）进展的病理生理中的作用已被重新审视。越来越多的证据在此进行了综述，归因于肥大病和坏死病对AKI，肾单位丢失和急性肾小管坏死起着重要的病理生理作用。我们将介绍在肥大症期间肾小管非细胞自主方式的概念，这种现象我们称为“死亡波”。我们假设坏死性坏死病可能通过肥大症引起细胞死亡的传播。剩余的坏死碎片需要有效的清除过程，以防止继发性炎症反应（称为坏死性炎症）。