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

Abstract

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.

Hederasaponin C inhibits LPS‐induced acute kidney injury in mice by targeting TLR4 and regulating the PIP2/NF‐κB/NLRP3 signaling pathway

“…This inflammasome, upon activation, overexpresses cleaved caspase-1 and mature IL-1β, resulting in NEU recruitment and the consequent progression of AKI (Danielski et al, 2020). Our results suggested that HSC decreased the expression to the AKI-associated inflammatory response (Gupta et al, 2020).…”

“…In addition, HSC inhibited the serum and kidney production of pro‐inflammatory cytokines TNF‐α, IL‐6, and IL‐1β in LPS‐stimulated AKI. TLR4 is proven to govern the PIP2 pathway, influencing the release of intracellular calcium and contributing to the AKI‐associated inflammatory response (Gupta et al, 2020). We observed that TAK‐242 could inhibit PIP2 and PLCγ2 protein expression.…”