Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate Sepsis-Induced Acute Kidney Injury by Promoting Mitophagy of Renal Tubular Epithelial Cells via the SIRT1/Parkin Axis

Guo, Jun; Wang, Rong; Liu, Donghai

doi:10.3389/fendo.2021.639165

Cited by 49 publications

(31 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Guo et al ( 115 ) and Liu et al ( 116 ) found that apoptosis and pyroptosis coexist in CLP mice. Li and Liu confirmed the same results ( 117 , 118 ). Yu et al ( 108 ) found that autophagy existed in a CLP mouse model, in the early stage, autophagy was stronger, and gradually weakened over time.…”

Section: Relationship Between Various Types Programmed Cell Deathsupporting

confidence: 73%

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Deng

Zhou

et al. 2022

Front. Med.

View full text Add to dashboard Cite

Sepsis-associated acute kidney injury (SA-AKI) is common in patients with severe sepsis, and has a high incidence rate and high mortality rate in ICU patients. Most patients progress to AKI before drug treatment is initiated. Early studies suggest that the main mechanism of SA-AKI is that sepsis leads to vasodilation, hypotension and shock, resulting in insufficient renal blood perfusion, finally leading to renal tubular cell ischemia and necrosis. Research results in recent years have shown that programmed cell death such as apoptosis, necroptosis, pyroptosis and autophagy play important roles. In the early stage of sepsis-related AKI, autophagy bodies form and inhibit various types of programmed cell death. With the progress of disease, programmed cell death begins. Apoptosis promoter represents caspase-8-induced apoptosis and apoptosis effector represents caspase-3-induced apoptosis, however, caspase-11 and caspase-1 regulate gasdermin D-mediated pyroptosis. Caspase-8 and receptor interacting kinase 1 bodies mediate necroptosis. This review focuses on the pathophysiological mechanisms of various programmed cell death in sepsis-related AKI.

show abstract

Section: Relationship Between Various Types Programmed Cell Deathsupporting

confidence: 73%

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Deng

Zhou

et al. 2022

Front. Med.

View full text Add to dashboard Cite

show abstract

“…To study how miR-30b-5p participated in the regulation of autophagy, the targeted binding sites between miR-30b-5p and SIRT1 were predicted through the bioinformatics online website Transtarget 7.2 ( Figure 3A ). The regulation of SIRT1 in autophagy is repeatedly reported ( 23 , 24 , 35 ). The binding relationship between miR-30b-5p and SIRT1 was elucidated by a dual-luciferase assay ( Figure 3B ).…”

Section: Resultsmentioning

confidence: 82%

Baicalein Induces Mitochondrial Autophagy to Prevent Parkinson's Disease in Rats via miR-30b and the SIRT1/AMPK/mTOR Pathway

et al. 2022

View full text Add to dashboard Cite

Parkinson's disease (PD) is a prevailing neurodegenerative disorder. Baicalein has neuroprotective effects on PD animals, but its mechanism is not clarified. We explored baicalein effects on PD rats. PD rat models were established by injecting 6-hydroxydopamine into the striatum of substantia nigra on the left side of the rat brain and treated with baicalein. Dopamine (DA) content, neuronal apoptosis, neuronal injury, neuronal mitochondria, and autophagy were assessed. Baicalein-treated PD rats were treated with autophagy inhibitor 3-methyladenine to identify the role of autophagy in PD. PD rats were injected with AgomiR-30b-5p or sh-SIRT1 plasmids and treated with baicalein. PD rats elicited decreased neurological score and DA secretion of the striatum, increased neuronal apoptosis, and injury, and reduced number of mitochondria and autophagy, whereas baicalein alleviated neuronal injury and partly recovered mitochondrial dysfunction, 3-methyladenine inhibited the protection of baicalein. miR-30b-5p was elevated and SIRT1 was diminished in PD rats and inhibited by baicalein. miR-30b-5p targeted SIRT1. miR-30b-5p overexpression or SIRT1 silencing annulled the protection of baicalein. The phosphorylation level of AMPK in the substantia nigra of PD rats was decreased and mTOR was increased, whereas baicalein annulled these trends. Briefly, baicalein activated mitochondrial autophagy via miR-30b-5p and the SIRT1/AMPK/mTOR pathway, thus protecting PD rats.

show abstract

“…MSCs play a protective role in mitochondria for renal repair mainly through the following mechanisms: 1) transfer of mitochondria to damaged proximal tubular epithelial cells ( Konari et al, 2019 ); 2) regulation of mitochondrial biogenesis by enhancing PGC1-α expression, NAD + biosynthesis, and SIRT3 activity ( Perico et al, 2017 ); 3) inhibition of mitochondria-mediated apoptosis and mitophagy (in hexavalent chromium-injured kidney) ( Yin et al, 2019 ); and 4) activation of mitophagy (in sepsis- and cisplatin-induced AKI) ( Wang et al, 2017 ; Guo et al, 2021 ). Recent studies have indicated that MSC-EVs also have a protective effect on mitochondrial damage caused by AKI, which protects TECs against injury by reducing mitochondrial fragmentation, normalizing mitochondrial membrane potential, and reversing mitochondrial DNA deletion and oxidative phosphorylation defects ( Cao et al, 2020 ; Zhao et al, 2021 ).…”

Section: Fatty Acid β-Oxidation and Stem Cell-based Therapymentioning

confidence: 99%

Fatty Acid β-Oxidation in Kidney Diseases: Perspectives on Pathophysiological Mechanisms and Therapeutic Opportunities

Gao

Chen

2022

Front. Pharmacol.

View full text Add to dashboard Cite

The kidney is a highly metabolic organ and requires a large amount of ATP to maintain its filtration-reabsorption function, and mitochondrial fatty acid β-oxidation serves as the main source of energy to meet its functional needs. Reduced and inefficient fatty acid β-oxidation is thought to be a major mechanism contributing to kidney diseases, including acute kidney injury, chronic kidney disease and diabetic nephropathy. PPARα, AMPK, sirtuins, HIF-1, and TGF-β/SMAD3 activation have all been shown to play key roles in the regulation of fatty acid β-oxidation in kidney diseases, and restoration of fatty acid β-oxidation by modulation of these molecules can ameliorate the development of such diseases. Here, we disentangle the lipid metabolism regulation properties and potential mechanisms of mesenchymal stem cells and their extracellular vesicles, and emphasize the role of mesenchymal stem cells on lipid metabolism. This review aims to highlight the important role of fatty acid β-oxidation in the progression of kidney diseases, and to explore the fatty acid β-oxidation effects and therapeutic potential of mesenchymal stem cells for kidney diseases.

show abstract

Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate Sepsis-Induced Acute Kidney Injury by Promoting Mitophagy of Renal Tubular Epithelial Cells via the SIRT1/Parkin Axis

Cited by 49 publications

References 53 publications

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Baicalein Induces Mitochondrial Autophagy to Prevent Parkinson's Disease in Rats via miR-30b and the SIRT1/AMPK/mTOR Pathway

Fatty Acid β-Oxidation in Kidney Diseases: Perspectives on Pathophysiological Mechanisms and Therapeutic Opportunities

Contact Info

Product

Resources

About