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Acute Kidney Injury and Cytokines

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Acute Kidney Injury and Regenerative Medicine

Abstract

Cytokines and chemokines are potential signaling molecules that maintain homeostasis by activating intracellular communication. Cytokines orchestrate various processes, ranging from cellular survival, proliferation, and chemotaxis for tissue repair to regulation of inflammation. Extracellular vesicles (EVs), which are cell-derived membrane particles such as exosomes and microvesicles, may also play crucial roles similar to cytokines. The kidneys are highly susceptible to intrinsic oxidative stress resulting from ischemia and to the excessive inflammatory response resulting from systemic autoimmunity. These types of stress may eventually result in the development of acute kidney injury (AKI). In this setting, the skewed cytokine profile produced by macrophages and lymphocytes disrupts the reciprocal relationship for regulating tissue repair and remodeling due to amplification of a physiological vicious loop. We have so far shown that AKI induces the secretion of midkine (MK) and CD147/basigin, which are responsible for skewed cytokine production. MK and CD147/basigin secreted by tubular epithelial cells promote the recruitment of macrophages and neutrophils, respectively, which are accompanied by monocyte chemotactic protein-1, transforming growth factor-β, E cadherin, and extracellular matrix metalloproteinase inducer.

This chapter will present the functions of macrophage-related cytokines and EVs and summarize our findings on how MK and CD147/basigin are involved in the pathogenesis of AKI.

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Furuhashi, K., Kato, N., Kosugi, T., Maruyama, S. (2020). Acute Kidney Injury and Cytokines. In: Terada, Y., Wada, T., Doi, K. (eds) Acute Kidney Injury and Regenerative Medicine . Springer, Singapore. https://doi.org/10.1007/978-981-15-1108-0_23

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