The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
miR-129-5p alleviates LPS-induced acute kidney injury via targeting HMGB1/TLRs/NF-kappaB pathway
Abstract
Introduction The present study aimed to investigate whether miR-129-5p can regulate high-mobility group box protein 1 (HMGB1)-modulated TLRs/NF-kappaB inflammatory pathway that contributed to lipopolysaccharide (LPS)-induced podocyte apoptosis and acutekidneyinjury (AKI). Material and methods In vitro and in vivo models of sepsis were simulated using LPS-administrated podocytes and mice, respectively. The effects of LPS, mR-129-5p mimics and short hairpin RNA of HMGB1 (sh-HMGB1) on podocyte apoptosis were monitored using TUNEL staining. Protein expression was measured using western blotting. Survival outcomes were analyzed in septic mice with agomir-mR-129-5p administration. Results We observed that stimulation of podocytes with LPS significantly inhibits the expression of miR-129-5p, and overexpression of miR-129-5p protects against LPS-induced podocyte damage, over-activation of inflammatory response and apoptosis. In a mouse model, agomir-miR-129-5p administration significantly improves the survival outcomes in septic mice and LPS-induced AKI. Mechanically, LPS-induced the elevation of HMGB1, TLR2, TLR4 and nuclear NF-κB protein expression in vitro and in vivo are restrained by the overexpression of miR-129-5p. Conclusions Overexpression of miR-129-5p protects against LPS-induced podocyte apoptosis, inflammation and AKI in vivo and in vitro models of sepsis. The underlying molecular mechanism is mediated via attenuating HMGB1/TLRs/NF-κB signaling axis modulated inflammator…
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“In line with these observations, decreased levels of miR-129-5p have been associated with the induction of inflammatory processes in various other diseases such as kidney injury or rheumatoid arthritis [59, 84].”
From A role for astrocytic miR-129-5p in frontotemporal dementia (2025) · cites this paper as [59]
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2 retracted
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Retracted(2019) · Journal of Cellular Biochemistry · doi:10.1002/jcb.28409 · Cited by 40
RetractedHMG-1 as a Late Mediator of Endotoxin Lethality in Mice
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Sepsis associated acute kidney injury
Poston, J. T., & Koyner, J. L. (2019) · BMJ · doi:10.1136/bmj.k4891 · Cited by 818
The Endotoxin Delivery Protein HMGB1 Mediates Caspase-11-Dependent Lethality in Sepsis
Deng, M., Tang, Y., Li, W., Wang, X., Zhang, R., Zhang, X., Zhao, X., Liu, J., Tang, C., Liu, Z., et al. (2018) · Immunity · doi:10.1016/j.immuni.2018.08.016 · Cited by 591
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Autophagy in acute kidney injury
Kaushal, G. P., & Shah, S. V. (2016) · Kidney International · doi:10.1016/j.kint.2015.11.021 · Cited by 389
MD-2 is required for disulfide HMGB1–dependent TLR4 signaling
Yang, H., Wang, H., Ju, Z., Ragab, A. A., Lundbäck, P., Long, W., Valdes-Ferrer, S. I., He, M., Pribis, J. P., Li, J., et al. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20141318 · Cited by 375
High Mobility Group Box Protein 1 (HMGB1): The Prototypical Endogenous Danger Molecule
Yang, H., Wang, H., Chavan, S. S., & Andersson, U. (2015) · Molecular Medicine · doi:10.2119/molmed.2015.00087 · Cited by 357
Cited by
A role for astrocytic miR-129-5p in frontotemporal dementia
Kaurani, L., Pradhan, R., Schröder, S., Burkhardt, S., Schuetz, A.-L., Krüger, D. M., Pena, T., Heutink, P., Sananbenesi, F., & Fischer, A. (2025) · Translational Psychiatry · doi:10.1038/s41398-025-03338-y · Cited by 10
Metadata
- Authors
- Huang, X., Hou, X., Chuan, L., Wei, S., Wang, J., Yang, X., & Ru, J.
- Venue
- International Immunopharmacology
- Publisher
- Elsevier BV
- Published
- 2020-12
- Volume
- 89
- Pages
- 107016
- ISSN
- 1567-5769
- Cited by
- 47
- References
- 46
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
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- Huang, X., Hou, X., Chuan, L., Wei, S., Wang, J., Yang, X., & Ru, J. (2020). miR-129-5p alleviates LPS-induced acute kidney injury via targeting HMGB1/TLRs/NF-kappaB pathway. International Immunopharmacology. https://doi.org/10.1016/j.intimp.2020.107016
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