Abstract
Acute kidney injury (AKI) causes a lot of harm to human health but is treated by only supportive therapy in most cases. Recent evidence shows that mesenchymal stem cells (MSCs) benefit kidney regeneration through releasing paracrine factors and extracellular vesicles (EVs) to the recipient kidney cells and are considered to be promising cellular therapy for AKI. To develop more efficient, precise therapies for AKI, we review the therapeutic mechanism of MSCs and MSC-derived EVs in AKI and look for a better understanding of molecular signaling and cellular communication between donor MSCs and recipient kidney cells. We also review recent clinical trials of MSC-EVs in AKI. This review summarizes the molecular mechanisms of MSCs’ therapeutic effects on kidney regeneration, expecting to comprehensively facilitate future clinical application for treating AKI.
Highlights
The kidney is a victim of critical systemic illnesses, and Acute kidney injury (AKI) usually develops as a complication during hospitalization and is related to increased mortality
It suggests that these modulated miRNAs may be responsible for reducing kidney cell death through inhibiting ATP depletion [66]. Another evidence that miRNA transferred by extracellular vesicles (EVs) regulates kidney cells regeneration was from the study by Gu et al, who had identified that human Wharton Jelly mesenchymal stromal cells-EVs alleviated cell apoptosis via regulating dynamin-related protein1 (DRP1) expression and mitochondria fission through a miR-30-related anti-apoptotic mechanism
The renal tubular epithelial cells (TECs) didn’t express IL-10 initially and obtained the IL-10 messenger RNAs (mRNAs) and de novo IL-10 protein after co-culture with bone marrow-derived mesenchymal stem cell (MSC) (BM-MSCs)-EVs and ucMSC-EVs. These findings suggest EVs enhanced IL-10/IL-10R1R2 anti-inflammatory pathway via translated IL-10 mRNA, indicating that the therapeutic mRNAs in EVs provided a promising therapy for AKI [23]
Summary
The kidney is a victim of critical systemic illnesses, and AKI usually develops as a complication during hospitalization and is related to increased mortality. ↓macrophage infiltration ↓Tubular apoptosis, ↑tubular proliferation, Abbreviations: AKI, acute kidney injury; α-SMA,α-smooth muscle actin; BM-MSCs, bone marrow-derived MSCs; CDK1, cyclin-dependent kinases 1; DRP1, dynamin-related protein 1; EMT, epithelialmesenchymal transition; ERK, extracellular-signal-regulated kinase; EVs, extracellular vesicles; Exos, exosomes; HGF, hepatocyte growth factor; H/R, hypoxia/reoxygenation; hWJMSCs, human Wharton’s jelly-MSCs; hucMSCs, human umbilical cord MSCs; I/R, ischemia/reperfusion; IGF-1R, insulin-like growth factor-1 receptor; iPSC-MSCs, induced pluripotent stem cell-derived MSCs; IRAK1, interleukin-1 receptor-associated kinase; KMSC, kidney-derived MSCs; MSC, mesenchymal stem cell; MVs, microvesicles; NM, not mentioned; PCNA, proliferating cell nuclear antigen; PTECs, proximal tubular epithelial cells; S1P, sphinganine-1-phosphate; SK1, sphingosine kinase 1; SP1, specificity protein 1
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