Progression of chronic kidney disease to kidney fibrosis is a key challenge in nephrology. Several contributions from the past year have shed light not only on the general molecular signature of human kidney fibrosis, but also on specific new mechanisms involved in its development.
Key advances
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The combined use of omics tools has provided insights into the landscape of kidney fibrosis and identified fibrotic microenvironments and injury patterns that are predictive of disease progression1.
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Persistence of SOX9 signalling in injured tubule epithelial cells activates downstream pathways that promote maladaptive repair and contribute to progression of acute kidney injury to chronic kidney disease2.
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ADAMTS12 drives the early activation of injury-responsive fibroblasts, highlighting an important role for non-structural extracellular matrix proteins in fibrosis6.
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Adaptive metabolic responses to kidney injury influence the development of senescence and the activation of pro-fibrotic pathways9,10.
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References
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Acknowledgements
Grants: INNOREN âP2022/BMD-7221: Nuevas estrategias diagnósticas y terapéuticas en enfermedad renal crónicaâ and PID2022-136703OB-I00 funded by MCIN/AEI 10.13039/501100011033/FEDER, UE.
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Lamas, S., Ruiz-Ortega, M. Insights into the mechanisms of fibrosis and progressive kidney injury. Nat Rev Nephrol 21, 79â80 (2025). https://doi.org/10.1038/s41581-024-00922-1
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DOI: https://doi.org/10.1038/s41581-024-00922-1
