| Literature DB >> 35372990 |
Abstract
AKI remains highly prevalent, yet no optimal therapy is available to prevent it or promote recovery after initial insult. Experimental studies have demonstrated that both innate and adaptive immune responses play a central role during AKI. In response to injury, myeloid cells are first recruited and activated on the basis of specific signals from the damaged microenvironment. The subsequent recruitment and activation state of the immune cells depends on the stage of injury and recovery, reflecting a dynamic and diverse spectrum of immunophenotypes. In this review, we highlight our current understanding of the mechanisms by which myeloid cells contribute to injury, repair, and fibrosis after AKI.Entities:
Keywords: AKI; CKD; acute kidney injury and ICU nephrology; basic science; dendritic cell; fibrosis; kidney repair; macrophage; myeloid cell; neutrophil
Mesh:
Year: 2021 PMID: 35372990 PMCID: PMC8785849 DOI: 10.34067/KID.0000672021
Source DB: PubMed Journal: Kidney360 ISSN: 2641-7650