Therapeutic Potential of Mesenchymal Stem Cells in Cisplatin-Induced Acute Kidney Injury via ASK-1/TXNIP Pathway Modulation Article Swipe
Amal AbdEl-Aziz
,
Radwa Y. Mekky
,
Sherine M. Ibrahim
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.5114/aoms/193707
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.5114/aoms/193707
Introduction Acute kidney injury (AKI) is a diverse set of illnesses characterized by a rapid decline in kidney function Material and methods Characteristics and homing of MSCs to kidney tissues were identified by flow cytometry and differentiation capability. After AKI induction by cisplatin injection in sixteen albino rats, the AKI rats were further subdivided into three subgroups. The first subgroup served as a positive control and the second one received 2 mg/kg furosemide (FUR) which served as a standard drug. The third subgroup received a single dose of 5 x 106 MSCs via tail vein injection once a week for consecutive two weeks. AKI-related biochemical parameters were assayed at 2 weeks after MSC treatment. Kidney histological changes were also evaluated. Moreover, the apoptosis of kidney cells and expression of apoptosis-related proteins were assessed by western blot. Results Compared with AKI rats, rats treated with MSCs showed suppressed serum levels of creatinine and blood urea nitrogen. MSC treatment alleviated the pathological abnormalities in the kidneys of AKI rats as shown by H&E staining.Furthermore, MSC treatment suppressed apoptosis of kidney cells in AKI rats via downregulation of apoptotic proteins; thioredoxin-interacting protein (TXNIP) and apoptosis signal-regulating kinase 1 (ASK1). Most importantly, MSC treatment promoted the expression of vascular endothelial growth factor (VEGF) in the kidneys of AKI rats. Conclusions Our results suggest that MSCs could ameliorate renal injury of AKI rats via their antiapoptotic properties. Also, the protective effects of MSCs may be mediated by their angiogenic potential effects.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.5114/aoms/193707
- OA Status
- gold
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- OpenAlex ID
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All OpenAlex metadata
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- OpenAlex ID
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https://openalex.org/W4407853664Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.5114/aoms/193707Digital Object Identifier
- Title
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Therapeutic Potential of Mesenchymal Stem Cells in Cisplatin-Induced Acute Kidney Injury via ASK-1/TXNIP Pathway ModulationWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
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2024-11-02Full publication date if available
- Authors
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Amal AbdEl-Aziz, Radwa Y. Mekky, Sherine M. IbrahimList of authors in order
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https://doi.org/10.5114/aoms/193707Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
- OA URL
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https://doi.org/10.5114/aoms/193707Direct OA link when available
- Concepts
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Medicine, Mesenchymal stem cell, Acute kidney injury, Stem cell, Cancer research, Cisplatin, Ask price, Pharmacology, Bioinformatics, Cell biology, Internal medicine, Pathology, Chemotherapy, Biology, Economy, EconomicsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.homing | 24 |
| abstract_inverted_index.injury | 3, 224 |
| abstract_inverted_index.kidney | 2, 17, 28, 124, 177 |
| abstract_inverted_index.kinase | 193 |
| abstract_inverted_index.levels | 148 |
| abstract_inverted_index.second | 67 |
| abstract_inverted_index.served | 60, 75 |
| abstract_inverted_index.showed | 145 |
| abstract_inverted_index.single | 85 |
| abstract_inverted_index.weeks. | 102 |
| abstract_inverted_index.(ASK1). | 195 |
| abstract_inverted_index.(TXNIP) | 189 |
| abstract_inverted_index.H&E | 170 |
| abstract_inverted_index.Results | 136 |
| abstract_inverted_index.assayed | 107 |
| abstract_inverted_index.changes | 116 |
| abstract_inverted_index.control | 64 |
| abstract_inverted_index.decline | 15 |
| abstract_inverted_index.diverse | 7 |
| abstract_inverted_index.effects | 235 |
| abstract_inverted_index.further | 52 |
| abstract_inverted_index.kidneys | 163, 211 |
| abstract_inverted_index.methods | 21 |
| abstract_inverted_index.protein | 188 |
| abstract_inverted_index.results | 217 |
| abstract_inverted_index.sixteen | 45 |
| abstract_inverted_index.suggest | 218 |
| abstract_inverted_index.tissues | 29 |
| abstract_inverted_index.treated | 142 |
| abstract_inverted_index.western | 134 |
| abstract_inverted_index.Compared | 137 |
| abstract_inverted_index.Material | 19 |
| abstract_inverted_index.assessed | 132 |
| abstract_inverted_index.effects. | 245 |
| abstract_inverted_index.function | 18 |
| abstract_inverted_index.mediated | 240 |
| abstract_inverted_index.positive | 63 |
| abstract_inverted_index.promoted | 200 |
| abstract_inverted_index.proteins | 130 |
| abstract_inverted_index.received | 69, 83 |
| abstract_inverted_index.standard | 78 |
| abstract_inverted_index.subgroup | 59, 82 |
| abstract_inverted_index.vascular | 204 |
| abstract_inverted_index.Moreover, | 120 |
| abstract_inverted_index.apoptosis | 122, 175, 191 |
| abstract_inverted_index.apoptotic | 185 |
| abstract_inverted_index.cisplatin | 42 |
| abstract_inverted_index.cytometry | 34 |
| abstract_inverted_index.illnesses | 10 |
| abstract_inverted_index.induction | 40 |
| abstract_inverted_index.injection | 43, 95 |
| abstract_inverted_index.nitrogen. | 154 |
| abstract_inverted_index.potential | 244 |
| abstract_inverted_index.proteins; | 186 |
| abstract_inverted_index.treatment | 156, 173, 199 |
| abstract_inverted_index.alleviated | 157 |
| abstract_inverted_index.ameliorate | 222 |
| abstract_inverted_index.angiogenic | 243 |
| abstract_inverted_index.creatinine | 150 |
| abstract_inverted_index.evaluated. | 119 |
| abstract_inverted_index.expression | 127, 202 |
| abstract_inverted_index.furosemide | 72 |
| abstract_inverted_index.identified | 31 |
| abstract_inverted_index.parameters | 105 |
| abstract_inverted_index.protective | 234 |
| abstract_inverted_index.subdivided | 53 |
| abstract_inverted_index.subgroups. | 56 |
| abstract_inverted_index.suppressed | 146, 174 |
| abstract_inverted_index.treatment. | 113 |
| abstract_inverted_index.AKI-related | 103 |
| abstract_inverted_index.Conclusions | 215 |
| abstract_inverted_index.biochemical | 104 |
| abstract_inverted_index.capability. | 37 |
| abstract_inverted_index.consecutive | 100 |
| abstract_inverted_index.endothelial | 205 |
| abstract_inverted_index.properties. | 231 |
| abstract_inverted_index.Introduction | 0 |
| abstract_inverted_index.histological | 115 |
| abstract_inverted_index.importantly, | 197 |
| abstract_inverted_index.pathological | 159 |
| abstract_inverted_index.abnormalities | 160 |
| abstract_inverted_index.antiapoptotic | 230 |
| abstract_inverted_index.characterized | 11 |
| abstract_inverted_index.downregulation | 183 |
| abstract_inverted_index.Characteristics | 22 |
| abstract_inverted_index.differentiation | 36 |
| abstract_inverted_index.apoptosis-related | 129 |
| abstract_inverted_index.signal-regulating | 192 |
| abstract_inverted_index.staining.Furthermore, | 171 |
| abstract_inverted_index.thioredoxin-interacting | 187 |
| cited_by_percentile_year | |
| countries_distinct_count | 1 |
| institutions_distinct_count | 3 |
| citation_normalized_percentile.value | 0.46776221 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |