Abstract:
:Kidney aging leads to an increased incidence of end-stage renal disease (ESRD) in the elderly, and aging is a complex biological process controlled by signaling pathways and transcription factors. Podocyte senescence plays a central role in injury resulting from kidney aging. Here, we demonstrated the critical role of C/EBPα in podocyte senescence and kidney aging by generating a genetically modified mouse model of chronological aging in which C/EBPα was selectively deleted in podocytes and by overexpressing C/EBPα in cultured podocytes, in which premature senescence was induced by treatment with adriamycin. Moreover, we illuminated the mechanisms by which podocyte senescence causes tubular impairment by stimulating HK-2 cells with bovine serum albumin (BSA) and chloroquine. Our findings suggest that C/EBPα knockout in podocytes aggravates podocyte senescence through the AMPK/mTOR pathway, leading to glomerulosclerosis, and that subsequent albuminuria exacerbates the epithelial-mesenchymal transdifferentiation of senescent tubular cells by suppressing autophagy. These observations highlight the importance of C/EBPα as a new potential target in kidney aging.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Zhang L,Zhou F,Yu X,Zhu Y,Zhou Y,Liu J,Liu Y,Ma Q,Zhang Y,Wang W,Chen Ndoi
10.1038/s41419-019-1933-2subject
Has Abstractpub_date
2019-09-17 00:00:00pages
684issue
10issn
2041-4889pii
10.1038/s41419-019-1933-2journal_volume
10pub_type
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