ArticleAmerican journal of translational research2021
Effect of miR-132-3p on sepsis-induced acute kidney injury in mice via regulating HAVCR1/KIM-1.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Urinary exosomal miR-132-3p as a novel non‑invasive biomarker for kidney scarring in pediatric vesicoureteral reflux patients.BMC pediatrics · 2026Article
- Outer membrane vesicles hijack TIM-1 for cellular uptake.PLoS pathogens · 2026Article
- MicroRNA-132 Alleviates Ischemia-Reperfusion-Induced Neuronal Apoptosis by Targeting Mecp2 in Stroke Models.Neurotoxicity research · 2026Article
- RNA-based therapeutic opportunities for the treatment of kidney diseases.Nature reviews. Nephrology · 2026Review
- Sepsis-associated acute kidney injury in mice and humans elicits heterogeneous renal microvascular microRNA responses.Scientific reports · 2025Article
- Sigma-1 Receptor Rescues Autophagy Through AMPK/mTOR Signaling Pathway in Sepsis-Induced Acute Kidney Injury.International journal of general medicine · 2025Article
- Article
- Effects of mesencephalic astrocyte-derived neurotrophic factor on sepsis-associated acute kidney injury.World journal of emergency medicine · 2023Article
- MicroRNAs in septic acute kidney injury.Burns & trauma · 2023Article
- Prevention of LPS-Induced Acute Kidney Injury in Mice by Bavachin and Its Potential Mechanisms.Antioxidants (Basel, Switzerland) · 2022Article
- MiR-501-5p alleviates cardiac dysfunction in septic patients through targeting NR4A3 to prevent its binding with Bcl-2.Cell cycle (Georgetown, Tex.) · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effect of miR-132-3p and HAVCR1/kidney injury molecule (KIM)-1 on sepsis-induced acute kidney injury (AKI) in mice.
methodsOne hundred C57BL/6 mice were divided into five groups with 20 mice in each group: the normal group (normal mice), the model group (mice with sepsis), the miR-132-3p mimic group (miR-132-3p overexpression), the oe-HAVCR1/KIM-1 group (HAVCR1/KIM-1 overexpression), and the miR-132-3p mimic + oe-HAVCR1/KIM-1 group. Dual-luciferase reporter assay was performed to verify the targeting relationship between miR-132-3p and HAVCR1/KIM-1. The expressions of miR-132-3p and HAVCR1/KIM-1 in mice' kidneys, the levels of renal function markers, the expressions of apoptosis-associated proteins, the renal cell apoptosis rate, and the inflammatory factors in serum were all examined.
resultsWe found that miR-132-3p can target HAVCR1/KIM-1 and regulate its expression. Compared with the normal mice, the septic mice exhibited lower miR-132-3p level and higher HAVCR1/KIM-1 level (both P<0.05). Moreover, the septic mice had higher levels of cleaved caspase-3, Bax, blood urea nitrogen, creatinine, tumor necrosis factor-α, interleukin-1β, and interleukin-6, higher renal cell apoptosis rate, and lower Bcl-2 level than the normal mice (all P<0.05). MiR-132-3p overexpression could improve the renal function of the mice with sepsis and inhibit renal cell apoptosis and inflammatory progression, whereas HAVCR1/KIM1 overexpression exhibited an opposite effect and could block the renal protective effects of miR-132-3p overexpression on the septic mice.
conclusionMiR-132-3p overexpression can inhibit renal cell apoptosis and inflammatory progression via suppressing HAVCR1/KIM-1 expression, thereby exert renal protective effects on mice with sepsis.
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34377256PMC8340183W3191619470What OpenQuestion holds
Registered trials
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