Volume 14 Issue 8
Aug.  2024
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Yini Bao, Qiyuan Shan, Keda Lu, Qiao Yang, Ying Liang, Haodan Kuang, Lu Wang, Min Hao, Mengyun Peng, Shuosheng Zhang, Gang Cao. Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis[J]. Journal of Pharmaceutical Analysis, 2024, 14(8): 100933. doi: 10.1016/j.jpha.2024.01.001
Citation: Yini Bao, Qiyuan Shan, Keda Lu, Qiao Yang, Ying Liang, Haodan Kuang, Lu Wang, Min Hao, Mengyun Peng, Shuosheng Zhang, Gang Cao. Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis[J]. Journal of Pharmaceutical Analysis, 2024, 14(8): 100933. doi: 10.1016/j.jpha.2024.01.001

Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis

doi: 10.1016/j.jpha.2024.01.001
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This work was financially supported by the National Natural Science Foundation of China (Grant No.: 82204625), the Natural Science Foundation of Zhejiang Province (Grant Nos.: LQ23H280013 and LZ22H280001), the Chinese Medicine Research Program of Zhejiang Province (Program Nos.: 2021ZZ009, 2023ZR009, and 2021ZQ023), and the Youth Natural Science Program of Zhejiang Chinese Medical University (Program No.: 2021RCZXZK14). We appreciate the great help from the Pharmaceutical Research Center and Medical Research Center, Academy of Chinese Medical Sciences, Zhejiang Chinese Medical University.

  • Received Date: Nov. 09, 2023
  • Accepted Date: Jan. 02, 2024
  • Rev Recd Date: Dec. 20, 2023
  • Publish Date: Jan. 03, 2024
  • Renal fibrosis is a devastating consequence of progressive chronic kidney disease, representing a major public health challenge worldwide. The underlying mechanisms in the pathogenesis of renal fibrosis remain unclear, and effective treatments are still lacking. Renal tubular epithelial cells (RTECs) maintain kidney function, and their dysfunction has emerged as a critical contributor to renal fibrosis. Cellular quality control comprises several components, including telomere homeostasis, ubiquitin-proteasome system (UPS), autophagy, mitochondrial homeostasis (mitophagy and mitochondrial metabolism), endoplasmic reticulum (ER, unfolded protein response), and lysosomes. Failures in the cellular quality control of RTECs, including DNA, protein, and organelle damage, exert profibrotic functions by leading to senescence, defective autophagy, ER stress, mitochondrial and lysosomal dysfunction, apoptosis, fibroblast activation, and immune cell recruitment. In this review, we summarize recent advances in understanding the role of quality control components and intercellular crosstalk networks in RTECs, within the context of renal fibrosis.

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