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Updated: Jul 13, 2026
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Macrophage Membrane-Camouflaged Nanozymes for Combating the Oxidative Stress-Microvascular Perfusion Negative
Fan Xia1,2, Shanshan Xiang3, Yihe Qiu3
1Department of Ultrasound in Medicine, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China.
Abstract:
Oxidative stress plays a critical role in the pathogenesis of ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI), driving necrosis of proximal tubule cells, inflammation, and capillary rarefaction. Inadequate perfusion resulting from capillary rarefaction can, in turn, induce chronic tissue hypoxia and exacerbate ischemic acute tubular necrosis, leading to an "oxidative stress-microvascular perfusion" negative feedback that further aggravate kidney damage. In this study, a macrophage membrane-camouflaged manganese-based antioxidant nanozyme (MB@LM) is developed for targeted delivery and oxidative stress relief in AKI therapy. By inheriting macrophage surface proteins, MB@LM selectively targets damaged renal tissues that overexpress adhesion molecules like intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), facilitating enhanced accumulation at the injury site. The manganese-based nanozyme core provides antioxidant enzyme-mimicking activities, effectively reducing oxidative stress and inhibiting apoptosis. In IRI-induced AKI mouse model, MB@LM treatment significantly reduces renal damage, restores renal microvascular perfusion as assessed by ultrasound imaging, and alleviated inflammation, demonstrating remarkable therapeutic efficacy. Overall, MB@LM represents a promising targeted therapy for AKI, offering precise delivery, potent antioxidant protection, and anti-inflammatory effects to support renal recovery and improve outcomes for AKI.
Insights
A novel macrophage membrane-camouflaged nanozyme (MB@LM) effectively targets kidney injury, reducing oxidative stress and inflammation. This breakthrough offers promising therapeutic potential for acute kidney injury (AKI) recovery.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Renal Medicine
Background:
- Oxidative stress is a key driver in ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI), causing cell death and inflammation.
- Microvascular dysfunction and capillary rarefaction in AKI create a feedback loop that exacerbates kidney damage.
- Current therapies for AKI often lack targeted delivery and effective management of oxidative stress.
Purpose of the Study:
- To develop a targeted antioxidant nanozyme for AKI therapy.
- To investigate the efficacy of macrophage membrane-camouflaged manganese-based nanozyme (MB@LM) in an IRI-induced AKI mouse model.
- To evaluate MB@LM's ability to reduce oxidative stress, inflammation, and improve renal microvascular perfusion.
Main Methods:
- Fabrication of a macrophage membrane-camouflaged manganese-based nanozyme (MB@LM).
- MB@LM was designed to target renal tissues overexpressing ICAM-1 and VCAM-1.
- Evaluation of MB@LM's antioxidant and anti-apoptotic activities in vitro and in vivo.
- Assessment of therapeutic efficacy in an IRI-induced AKI mouse model, including renal damage, microvascular perfusion (ultrasound imaging), and inflammation markers.
Main Results:
- MB@LM demonstrated selective targeting of damaged renal tissues.
- The nanozyme effectively mimicked antioxidant enzymes, reducing oxidative stress and apoptosis.
- Treatment with MB@LM significantly attenuated renal damage and inflammation in the AKI mouse model.
- Restoration of renal microvascular perfusion was observed following MB@LM treatment.
Conclusions:
- MB@LM serves as a promising targeted therapeutic agent for AKI.
- The nanozyme provides potent antioxidant and anti-inflammatory effects, aiding renal recovery.
- MB@LM's ability to restore microvascular perfusion highlights its potential to break the negative feedback loop in AKI pathogenesis.
