Sensory Nerve Signal Limits Kidney Ischemia–Reperfusion Injury in Mouse Models
Published in Immunology, Ischemia, Journals.
Published October 25, 2026.
A study in Cell Research identifies a protective interaction between sensory nerves and immune cells in experimental kidney ischemia–reperfusion injury, which occurs when blood flow is interrupted and then restored.
Lei Wang and colleagues mapped sensory fibers throughout kidney tissue using tissue clearing and three-dimensional imaging. In mouse experiments, removing TRPV1-positive sensory neurons worsened kidney dysfunction, tissue injury and fibrosis, whereas chemogenetic activation was protective.
The researchers traced part of this protection to calcitonin gene-related peptide (CGRP). This nerve-derived signal acts on monocytes and macrophages through the CALCRL–RAMP1 receptor complex and cAMP–PKA signaling, reducing inflammatory signals and myeloid-cell infiltration.
The team also found lower renal CGRP abundance in human samples from older adults and people with diabetes, with corresponding observations in mouse models. Exogenous CGRP reduced experimental injury particularly effectively in those vulnerable mouse settings.
Human tissue observations do not establish treatment efficacy. The protective intervention results are preclinical, and the work does not demonstrate that CGRP administration safely prevents acute kidney injury or chronic kidney disease in patients.