Cockayne syndrome is a genetic disease characterized by impairment of DNA repair mechanisms, premature ageing, cachexia and kidney dysfunction. New research in a mouse model of Cockayne syndrome demonstrates that injury induces a subset of kidney proximal tubule cells to express the anorexigenic peptide GDF15. These findings link kidney injury to cachexia and highlight the role of the kidney in mediating inter-organ homeostasis.
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PRDM16 acts as a homeostasis regulation factor to suppress the transition of AKI to CKD via upregulation of eukaryotic initiation factor 6
Cellular and Molecular Life Sciences Open Access 23 June 2025
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References
Heerspink, H. J. L. et al. Dapagliflozin in patients with chronic kidney disease. N. Engl. J. Med. 383, 1436–1446 (2020).
DeFronzo, R. A., Reeves, W. B. & Awad, A. S. Pathophysiology of diabetic kidney disease: impact of SGLT2 inhibitors. Nat. Rev. Nephrol. 17, 319–334 (2021).
Mulderrig, L. et al. Aldehyde-driven transcriptional stress triggers an anorexic DNA damage response. Nature 600, 158–163 (2021).
Solagna, F. et al. Pro-cachectic factors link experimental and human chronic kidney disease to skeletal muscle wasting programs. J. Clin. Invest. 131, e135821 (2021).
Schödel, J. & Ratcliffe, P. J. Mechanisms of hypoxia signalling: new implications for nephrology. Nat. Rev. Nephrol. 15, 641–659 (2019).
Patel, S. et al. GDF15 provides an endocrine signal of nutritional stress in mice and humans. Cell Metab. 29, 707–718.e8 (2019).
Scholz, H. et al. Kidney physiology and susceptibility to acute kidney injury: implications for renoprotection. Nat. Rev. Nephrol. 17, 335–349 (2021).
Sears, S. & Siskind, L. Potential therapeutic targets for cisplatin-induced kidney injury: lessons from other models of AKI and fibrosis. J. Am. Soc. Nephrol. 32, 1559–1567 (2021).
Braun, F. et al. SARS-CoV-2 renal tropism associates with acute kidney injury. Lancet 396, 597–598 (2020).
Sen, T. et al. Association between circulating GDF-15 and cardio-renal outcomes and effect of canagliflozin: results from the CANVAS trial. J. Am. Heart Assoc. 10, e021661 (2021).
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Puelles, V.G., Huber, T.B. Kidneys control inter-organ homeostasis. Nat Rev Nephrol 18, 207–208 (2022). https://doi.org/10.1038/s41581-022-00549-0
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DOI: https://doi.org/10.1038/s41581-022-00549-0
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PRDM16 acts as a homeostasis regulation factor to suppress the transition of AKI to CKD via upregulation of eukaryotic initiation factor 6
Cellular and Molecular Life Sciences (2025)
