Neuroimmune Mechanisms in Signaling of Pain During Acute Kidney Injury (AKI)

Frontiers in Medicine

article

Aprajita Gupta¹  Dev Kumar²  Sanjeev Puri³  Veena Puri¹ 

[1] Centre for Systems Biology & Bioinformatics, Panjab University;Department of Biochemistry, Postgraduate Institute of Medical Education and Research;Department of Biotechnology, University Institute of Engineering and Technology, Panjab University

关键词: acute kidney injury;    neuroinflammation;    pain;    neuropeptides;    CGRP;    TNF-α;    inflammation;   

DOI  :  10.3389/fmed.2020.00424

学科分类：社会科学、人文和艺术（综合）

来源: Frontiers

【 摘 要 】

Acute kidney injury (AKI) is a significant global health concern. The primary causes of AKI include ischemia, sepsis and nephrotoxicity. The unraveled interface between nervous system and immune response with specific focus on pain pathways is generating a huge interest in reference to AKI. The nervous system though static executes functions by nerve fibers throughout the body. Neuronal peptides released by nerves effect the immune response to mediate the hemodynamic system critical to the functioning of kidney. Pain is the outcome of cellular cross talk between nervous and immune systems. The widespread release of neuropeptides, neurotransmitters and immune cells contribute to bidirectional neuroimmune cross talks for pain manifestation. Recently, we have reported pain pathway genes that may pave the way to better understand such processes during AKI. An auxiliary understanding of the functions and communications in these systems will lead to novel approaches in pain management and treatment through the pathological state, specifically during acute kidney injury.

【 授权许可】

CC BY