journal article·2024-11-13

Lipid Nanoparticle-Mediated Oip5-as1 Delivery Preserves Mitochondrial Function in Myocardial Ischemia/Reperfusion Injury by Inhibiting the p53 Pathway

Xiaowei Niu, Jing Zhang, Jingjing Zhang, Lu Bai, Shuwen Hu, Zheng Zhang, Ming Bai

ACS Applied Materials & Interfaces· Volume 16· Issue 45
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Abstract

Myocardial ischemia/reperfusion (MI/R) injury, a major contributor to poor prognosis in patients with acute myocardial infarction, currently lacks effective therapeutic strategies in clinical practice. The long noncoding RNA (lncRNA) Oip5-as1 can regulate various cellular processes, such as cell proliferation, differentiation, and survival. Oip5-as1 may have potential as a therapeutic target for MI/R injury as its upregulated expression has been associated with reduced infarct size and improved cardiac function in animal models, although how to effectively and safely overexpress Oip5-as1 in vivo remains unclear. Lipid nanoparticles (LNPs) are a versatile technology for targeted drug delivery in numerous therapeutic applications. Herein, we aimed to assess the therapeutic efficacy and safety of LNPs coloaded with Oip5-as1 and a cardiomyocyte-specific binding peptide (LNP@Oip5-as1@CMP) in a murine model of MI/R injury. To achieve this, LNP@Oip5-as1@CMP was synthesized via ethanol injection method. The structural components of LNP@Oip5-as1@CMP were physicochemically analyzed. A hypoxia/reoxygenation (H/R) model in HL-1 cells and coronary artery ligation in mice were used to simulate MI/R injury. Our results demonstrated that LNPs designed for cardiomyocyte targeting and efficient Oip5-as1 delivery were successfully synthesized. In HL-1 cells, LNP@Oip5-as1@CMP treatment significantly reduced mitochondrial apoptosis caused by H/R injury. In the murine MI/R model, the intravenous administration of LNP@Oip5-as1@CMP significantly decreased myocardial infarct size and improved cardiac function. Mechanistic investigations revealed that Oip5-as1 delivery inhibited the p53 signaling pathway. However, the cardioprotective effects of Oip5-as1 were abrogated by administrating Nutlin-3a, a p53 activator. Furthermore, no signs of major organ damage were detected after LNP@Oip5-as1@CMP injection. Our study reveals the therapeutic potential of LNPs for targeted Oip5-as1 delivery in mitigating MI/R injury. These findings pave the way for advanced targeted treatments in cardiovascular diseases, emphasizing the promise of lncRNA-based therapies.
Source: openalex_inverted_index · Quality: baseline

Research context

OpenAlex topics: Cell death mechanisms and regulation · interferon and immune responses · Mitochondrial Function and Pathology

SciVX discovery tags are terminology-based. OpenAlex topics are source-provided classifications.

Affiliations

Department of Cardiology, The First Hospital of Lanzhou University; Gansu Key Laboratory of Cardiovascular Diseases; Gansu Clinical Medical Research Center for Cardiovascular Diseases, The First School of Clinical Medicine of Lanzhou University, No. 1, Donggang West Road, Chengguan District, Lanzhou, Gansu 730000, China

Medical Genetics Center, Gansu Provincial Central Hospital/Gansu Provincial Maternity and Child-Care Hospital, Gansu Provincial Clinical Research Center for Birth Defects and Rare Diseases, No. 143, North Road, Qilihe District, Lanzhou, Gansu 730000, China

Funding

Health Commission of Gansu Province · Gansu Education Department · Lanzhou Science and Technology Bureau · Science and Technology Department of Gansu Province · Special Fund for Civil-Military Integration Development of Gansu Province · Lanzhou University First Hospital

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