Exosomes Highlight Future Directions in the Treatment of Acute Kidney Injury.
Xiaoyu ZhangJing WangJing ZhangYuwei TanYiming LiZhiyong PengPublished in: International journal of molecular sciences (2023)
Acute kidney injury (AKI) is a severe health problem associated with high morbidity and mortality rates. It currently lacks specific therapeutic strategies. This review focuses on the mechanisms underlying the actions of exosomes derived from different cell sources, including red blood cells, macrophages, monocytes, mesenchymal stem cells, and renal tubular cells, in AKI. We also investigate the effects of various exosome contents (such as miRNA, lncRNA, circRNA, mRNA, and proteins) in promoting renal tubular cell regeneration and angiogenesis, regulating autophagy, suppressing inflammatory responses and oxidative stress, and preventing fibrosis to facilitate AKI repair. Moreover, we highlight the interactions between macrophages and renal tubular cells through exosomes, which contribute to the progression of AKI. Additionally, exosomes and their contents show promise as potential biomarkers for diagnosing AKI. The engineering of exosomes has improved their clinical potential by enhancing isolation and enrichment, target delivery to injured renal tissues, and incorporating small molecular modifications for clinical use. However, further research is needed to better understand the specific mechanisms underlying exosome actions, their delivery pathways to renal tubular cells, and the application of multi-omics research in studying AKI.
Keyphrases
- acute kidney injury
- mesenchymal stem cells
- induced apoptosis
- cardiac surgery
- stem cells
- oxidative stress
- cell cycle arrest
- umbilical cord
- endoplasmic reticulum stress
- cell therapy
- signaling pathway
- single cell
- cell death
- healthcare
- red blood cell
- high glucose
- gene expression
- machine learning
- dna damage
- endothelial cells
- mental health
- cell proliferation
- immune response
- dendritic cells
- climate change
- big data
- risk assessment
- binding protein
- pi k akt
- heat shock protein