Ischemia Reperfusion Injury: Opportunities for Nanoparticles

Zang, Xinlong; Zhou, Jingyi; Zhang, Xiaoxu; Han, Yantao; Chen, Xuehong

doi:10.1021/acsbiomaterials.0c01197

Cited by 25 publications

(17 citation statements)

References 112 publications

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“…Myocardial IRI (MIRI) is a severe pathophysiological condition associated with complex mechanisms, including oxidative stress, cell apoptosis, and inflammatory responses [ 5 , 6 , 7 ]. Overproduction of ROS activates various molecular cascades of apoptosis [ 8 , 9 ].…”

Section: Nrf2/keap1/are Pathway As a Potential Target In Iri Therapymentioning

confidence: 99%

“…IRI injury is a sequential catastrophic event with high morbidity and mortality, usually seen after thoracoabdominal surgeries, cardiopulmonary bypass, hemorrhagic, traumatic, or septic shock, severe burns, or after transplantation operations [ 1 ] characterized by loss of blood flow, causing hypoxia and lack of nutrition (ischemia phase) followed by restoration of the blood supply (reperfusion phase), which often results in systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) [ 2 , 3 , 4 , 5 , 6 ]. Interruption of the blood flow causes reduced oxygen-dependent-ATP production, impaired ion-pump activities, hypoxanthine and lactate accumulation (acidosis), intracellular calcium overload, which triggers reactive oxygen species (ROS) production.…”

Section: Introductionmentioning

confidence: 99%

“…It also activates calpains leading to programmed cell death, ROS production from previously sequestered hypoxanthine consequent to reoxygenation, thereby results in a positive feedback loop by opening the mitochondrial permeability transition pores (mPTP) to produce more ROS. Eventually, excess amounts of ROS result in oxidative stress and oxidase proteins, lipids, and DNA [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, ROS accumulation during I/R surpasses autophagic clearance capacity and eventually leads to cell death [ 3 , 6 ]. It has already been known that the disproportionate generation of ROS is the crucial mechanism underlying IRI [ 2 , 3 , 4 , 5 , 6 , 7 ]. This excessive ROS and RNS accumulation are kept down by water- and liposoluble antioxidants like glutathione and liposoluble vitamins, as well as antioxidant enzymes.…”

Section: Introductionmentioning

confidence: 99%

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Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Uçar

Saha³

et al. 2021

Antioxidants

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Ischemia/reperfusion (I/R) injury is associated with substantial clinical implications, including a wide range of organs such as the brain, kidneys, lungs, heart, and many others. I/R injury (IRI) occurs due to the tissue injury following the reestablishment of blood supply to ischemic tissues, leading to enhanced aseptic inflammation and stimulation of oxidative stress via reactive oxygen and nitrogen species (ROS/RNS). Since ROS causes membrane lipids’ peroxidation, triggers loss of membrane integrity, denaturation of proteins, DNA damage, and cell death, oxidative stress plays a critical part in I/R pathogenesis. Therefore, ROS regulation could be a promising therapeutic strategy for IRI. In this context, Nrf2 (NF-E2-related factor 2) is a transcription factor that regulates the expression of several factors involved in the cellular defense against oxidative stress and inflammation, including heme oxygenase-1 (HO-1). Numerous studies have shown the potential role of the Nrf2/HO-1 pathway in IRI; thus, we will review the molecular aspects of Nrf2/Kelch-like ECH-associated protein 1 (Keap1)/antioxidant response element (ARE) signaling pathway in I/R, and we will also highlight the recent insights into targeting this pathway as a promising therapeutic strategy for preventing IRI.

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Section: Nrf2/keap1/are Pathway As a Potential Target In Iri Therapymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Uçar

Saha³

et al. 2021

Antioxidants

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“…Tissue and cell damage after ischemic stroke and reperfusion leads to the production of reactive oxygen species (ROS), activating apoptosis, necrosis, and autophagy pathways that worsen the injury. In this regard, nanomedicine has contributed substantially to this field by developing NPs with antioxidant treatment cargos [83,84].…”

Section: Oxidative Stressmentioning

confidence: 99%

New Approaches in Nanomedicine for Ischemic Stroke

Correa-Paz

Silva‐Candal²,

Polo

et al. 2021

Pharmaceutics

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Ischemic stroke, caused by the interruption of blood flow to the brain and subsequent neuronal death, represents one of the main causes of disability in developed countries. Therapeutic methods such as recanalization approaches, neuroprotective drugs, or recovery strategies have been widely developed to improve the patient’s outcome; however, important limitations such as a narrow therapeutic window, the ability to reach brain targets, or drug side effects constitute some of the main aspects that limit the clinical applicability of the current treatments. Nanotechnology has emerged as a promising tool to overcome many of these drug limitations and improve the efficacy of treatments for neurological diseases such as stroke. The use of nanoparticles as a contrast agent or as drug carriers to a specific target are some of the most common approaches developed in nanomedicine for stroke. Throughout this review, we have summarized our experience of using nanotechnology tools for the study of stroke and the search for novel therapies.

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Ischemic Microenvironment‐Responsive Therapeutics for Cardiovascular Diseases

Zhang

Ren

et al. 2021

Advanced Materials

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Cardiovascular diseases caused by ischemia are attracting considerable attention owing to its high morbidity and mortality worldwide. Although numerous agents with cardioprotective benefits have been identified, their clinical outcomes are hampered by their low bioavailability, poor drug solubility, and systemic adverse effects. Advances in nanoscience and nanotechnology provide a new opportunity to effectively deliver drugs for treating ischemia‐related diseases. In particular, cardiac ischemia leads to a characteristic pathological environment called an ischemic microenvironment (IME), significantly different from typical cardiac regions. These remarkable differences between ischemic sites and normal tissues have inspired the development of stimuli‐responsive systems for the targeted delivery of therapeutic drugs to damaged cardiomyocytes. Recently, many biomaterials with intelligent properties have been developed to enhance the therapeutic benefits of drugs for the treatment of myocardial ischemia. Strategies for stimuli‐responsive drug delivery and release based on IME include reactive oxygen species, pH‐, hypoxia‐, matrix metalloproteinase‐, and platelet‐inspired targeting strategies. In this review, state‐of‐the‐art IME‐responsive biomaterials for the treatment of myocardial ischemia are summarized. Perspectives, limitations, and challenges are also discussed for the further development of innovative and effective approaches to treat ischemic diseases with high effectiveness and biocompatibility.

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Ischemia Reperfusion Injury: Opportunities for Nanoparticles

Cited by 25 publications

References 112 publications

Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

New Approaches in Nanomedicine for Ischemic Stroke

Ischemic Microenvironment‐Responsive Therapeutics for Cardiovascular Diseases

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