Cellular Stress and Immunity in Kidney Disease: Shared Mechanisms of Injury, Repair, and Cancer

Kidney cells are continuously exposed to ischemic, metabolic, toxic, and immunological stressors. These insults activate a conserved repertoire of stress-response pathways, including the integrated stress response and unfolded protein response, mitochondrial dysfunction, autophagy and mitophagy, cellular senescence, and regulated cell death such as ferroptosis and pyroptosis. This machinery is tightly interwoven with innate and adaptive immune signaling. Strikingly, the same molecular nodes persist across acute kidney injury, chronic kidney disease, transplant alloimmunity, infection, and renal malignancy, driving both injury and repair. Yet these mechanisms are usually studied within single-disease silos, obscuring the common ground that connects them.This Research Topic unites cellular-stress and immunology-focused kidney research across the disease spectrum to reveal shared mechanisms that transcend individual diagnoses. We place the stressed tubular epithelial cell at the center: under stress it shifts from a structural workhorse into an active driver of inflammation, fibrosis, and sometimes malignant transformation, and how it senses and responds to injury often determines whether the kidney recovers, progresses to chronic disease, or develops cancer. We aim to build a mechanistic picture of how tubular and immune cells respond to injury and metabolic shocks, how these responses can be redirected toward repair, and how immune cells either ameliorate or exacerbate renal cancer progression. By bringing together researchers working in acute, chronic, neoplastic, infectious, and transplant contexts, we seek common therapeutic targets and biomarkers and aim to accelerate translation of immune-directed interventions into the clinic.We welcome contributions on, but not limited to: - Conserved stress-response pathways (including ER stress/UPR, the integrated stress response, mitochondrial dysfunction, autophagy/mitophagy, senescence, and regulated cell death) in tubular and other renal cells- Immune-epithelial interactions during the AKI-to-CKD transition- The interface between cellular stress and innate/adaptive immunity (such as DAMPs, cGAS–STING, inflammasomes, interferons, complement, and macrophage or T-cell programs)- Immune mechanisms of renal recovery following ischemic, septic, toxic, and metabolic injury- Shared drivers of the AKI-to-CKD transition and renal fibrosis- The role of immune cells in either ameliorating or exacerbating renal cancer progressionWe invite Original Research, Review and Case Report articles spanning experimental models, human tissue, single-cell and spatial approaches, and translational or clinical studies. Topic editors: Sounak Ghosh Roy, Ph.D., Anand C Reghuvaran Nair, Manga Motrapu Source: https://www.frontiersin.org/research-topics/83567/cellular-stress-and-immunity-in-kidney-disease-shared-mechanisms-of-injury-repair-and-cancer