Apoptosis pathways in renal cells

Apoptosis pathways in renal cells encompass the complex signaling networks that regulate programmed cell death within the kidney's functional units, primarily the tubular epithelial cells and podocytes [1.1.1, 1.4.1]. These pathways are broadly categorized into the extrinsic (death receptor-mediated) and intrinsic (mitochondrial-mediated) pathways, both of which converge on the activation of executioner caspases like Caspase-3 [1.1.2, 1.4.1]. In the context of renal disease, excessive apoptosis is a hallmark of acute kidney injury (AKI) and chronic kidney disease (CKD), often triggered by ischemia, oxidative stress, or nephrotoxic drugs such as cisplatin and cyclosporine [1.2.1, 1.2.2]. Conversely, resistance to apoptosis is a key feature of renal cell carcinoma (RCC), where tumor cells evade death signals to promote survival and metastasis [1.3.1, 1.3.3]. Therapeutic strategies aim to either inhibit these pathways to preserve renal function in injury models or activate them to eliminate malignant cells in cancer [1.2.2, 1.4.2]. However, the clinical application of such therapies is challenged by the redundancy of cell death mechanisms, such as necroptosis and ferroptosis, and the potential for systemic side effects when modulating fundamental cell survival processes [1.4.3].

Other names

Renal apoptosisProgrammed cell death in renal cellsKidney cell apoptosis pathwaysRenal tubular cell apoptosis

Modulation of pro-apoptotic (e.g., Caspases, Bax) and anti-apoptotic (e.g., Bcl-2, IAPs) signaling cascades to regulate cell survival and death in renal tissues [1.2.2, 1.3.1, 1.4.1].