Cathepsin B in programmed cell death machinery: mechanisms of execution and regulatory pathways

Cell Death Dis. 2023 Apr 8;14(4):255. doi: 10.1038/s41419-023-05786-0.

Zhen Xie ^# ¹, Mengyuan Zhao ^# ¹, Chengxiang Yan ², Wei Kong ¹, Fei Lan ¹, Narengaowa ¹, Shuxuan Zhao ¹, Qinghu Yang ², Zhantao Bai ³ ⁴, Hong Qing ⁵, Junjun Ni ⁶

Affiliations

1 Key Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, 100081, Beijing, China.
2 Research Center for Resource Peptide Drugs, Shaanxi Engineering and Technological Research Center for Conversation and Utilization of Regional Biological Resources, Yan'an University, Yan'an, 716000, China.
3 Research Center for Resource Peptide Drugs, Shaanxi Engineering and Technological Research Center for Conversation and Utilization of Regional Biological Resources, Yan'an University, Yan'an, 716000, China. [email protected].
4 Yan'an Key Laboratory for Neural Immuno-Tumor and Stem Cell and Engineering and Technological Research Center for Natural Peptide Drugs, Yan'an, 716000, China. [email protected].
5 Key Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, 100081, Beijing, China. [email protected].
6 Key Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, 100081, Beijing, China. [email protected].
# Contributed equally.

PMID: 37031185 DOI: 10.1038/s41419-023-05786-0

Abstract

Cathepsin B (CatB), a cysteine protease, is primarily localized within subcellular endosomal and lysosomal compartments. It is involved in the turnover of intracellular and extracellular proteins. Interest is growing in CatB due to its diverse roles in physiological and pathological processes. In functional defective tissues, programmed cell death (PCD) is one of the regulable fundamental mechanisms mediated by CatB, including Apoptosis, Pyroptosis, Ferroptosis, Necroptosis, and autophagic cell death. However, CatB-mediated PCD is responsible for disease progression under pathological conditions. In this review, we provide an overview of the critical roles and regulatory pathways of CatB in different types of PCD, and discuss the possibility of CatB as an attractive target in multiple diseases. We also summarize current gaps in the understanding of the involvement of CatB in PCD to highlight future avenues for research.

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