Renal Nano-drug delivery for acute kidney Injury: Current status and future perspectives

Geo, Hui Nee; Murugan, Dharmani Devi; Chik, Zamri; Norazit, Anwar; Foo, Yiing Yee; Leo, Bey Fen; Teo, Yin Yin; Kadir, Sharifah Zamiah Syed Binti Syed Abdul; Chan, Yinghan; Chai, Hann Juang; Medel, María; Abdullah, Nor Azizan; Johns, Edward J.; Vicent, Marı́a J.; Chung, Lip Yong; Kiew, Lik Voon

doi:10.1016/j.jconrel.2022.01.033

Cited by 40 publications

(41 citation statements)

References 174 publications

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“…We prepared ROS-responsive NPS@Cur to study its effectiveness and protection of renal tubule epithelial from cisplatin-induced kidney injury. The structure and permeability of the injured glomerular filtration membrane changed at the initial stage of AKI and thus enabled NPs to pass through. , The size change of NPS (from 140.9 to 99.36 nm) facilitated accumulation in kidneys, because researchers have found that smaller nanoparticles were beneficial to accumulate in the injured kidney . The ex vivo fluorescence images and average counts collected from normal and AKI mice are showed in Figure A,B.…”

Section: Results and Discussionmentioning

confidence: 99%

“…Nanotechnology-based drug delivery systems have facilitated AKI therapy, such as early prevention, early diagnosis, drug delivery, and gene therapy. − In particular, stimulus-responsive polymeric drug delivery systems have attracted increasing attention for low toxicity, less side effects, prone accumulation into targeted tissues, and response to the disease microenvironment. − Liu et al synthesized a ROS-responsive prodrug based on chitosan-SS31 for AKI therapy. The prodrug presented ROS-responsive drug release leading to an enhanced therapeutic effect of SS31.…”

Section: Introductionmentioning

confidence: 99%

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Dual-Responsive Curcumin-Loaded Nanoparticles for the Treatment of Cisplatin-Induced Acute Kidney Injury

et al. 2022

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Acute kidney injury (AKI) has been a global public health concern leading to high patient morbidity and mortality in the world. Nanotechnology-mediated antioxidative therapy has facilitated the treatment of AKI. Herein, a hierarchical curcumin-loaded nanodrug delivery system (NPS@Cur) was fabricated for antioxidant therapy to ameliorate AKI. The nanoplatform could respond to subacidic and reactive oxygen species (ROS) microenvironments. The subacidic microenvironment led to a smaller size (from 140.9 to 99.36 nm) and positive charge (from −4.9 to 12.6 mV), contributing to the high accumulation of nanoparticles. An excessive ROS microenvironment led to nanoparticle degradation and drug release. In vitro assays showed that NPS@Cur could scavenge excessive ROS and relieve oxidative stress in H2O2-induced HK-2 cells through reduced apoptosis, activated autophagy, and decreased endoplasmic reticulum stress. Results from cisplatin-induced AKI models revealed that NPS@Cur could effectively alleviate mitochondria injury and protect kidneys via antioxidative protection, activated autophagy, decreased endoplasmic reticulum stress, and reduced apoptosis. NPS@Cur showed excellent biocompatibility and low toxicity to primary tissues in mice. These results revealed that NPS@Cur may be a potential therapeutic strategy for efficiently treating cisplatin or other cause-induced AKI.

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Section: Results and Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dual-Responsive Curcumin-Loaded Nanoparticles for the Treatment of Cisplatin-Induced Acute Kidney Injury

et al. 2022

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“…Importantly, the unique size and diverse surface modification strategies of nanodrugs provide significant advantages for their renal targeting. Currently, various component nanodrugs with various sizes and morphologies have been designed to accumulate in renal tissue for AKI antioxidant therapy [ 16 , [143] , [144] , [145] ] ( Fig. 9 A–B).…”

Section: Advantages Of Nanodrugs In Aki Treatmentmentioning

confidence: 99%

Nanodrugs alleviate acute kidney injury: Manipulate RONS at kidney

Chen

Nan

Yang

et al. 2023

Bioactive Materials

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“…10,11 (2) Oxidative stress injury: ATP is extensively degraded to hypoxanthine during renal ischemia and hypoxia, and hypoxanthine can further react with increased oxygen molecules during reperfusion, fueling the generation of massive amounts of reactive oxygen species (ROS). 12,13 Excessive ROS can not only damage organelle and plasma membranes, accelerating Ca 2+ influx via transmembrane ion transport perturbations, but also severely damage the structural functions of mitochondria and the endoplasmic reticulum (ER). 14 Sustained ER stress further induces large amounts of Ca 2+ to be rapidly released from calcium pools, disrupting the ER calcium balance and resulting in severe [Ca 2+ ] i dysregulation.…”

Section: Introductionmentioning

confidence: 99%

“…In I/R-induced AKI, a pathophysiological cascade is triggered, including intracellular calcium ion ([Ca 2+ ] i ) overload, oxidative stress, cellular energy metabolism disorder, and inflammatory response activation, in which the relationship among these mechanisms is intimately interwoven and plays pivotal roles in the pathological progression of AKI. Concrete mechanisms of kidney cell damage in the pathological process of AKI could include the following: (1) Intracellular Ca 2+ overload: During renal ischemia and hypoxia, the initial decrease in ATP causes depolarization of the cell membrane and activates the intracellular Na + –Ca 2+ exchange mechanism, which results in a massive extracellular Ca 2+ influx through the Ca 2+ channel. , (2) Oxidative stress injury: ATP is extensively degraded to hypoxanthine during renal ischemia and hypoxia, and hypoxanthine can further react with increased oxygen molecules during reperfusion, fueling the generation of massive amounts of reactive oxygen species (ROS). , Excessive ROS can not only damage organelle and plasma membranes, accelerating Ca 2+ influx via transmembrane ion transport perturbations, but also severely damage the structural functions of mitochondria and the endoplasmic reticulum (ER) . Sustained ER stress further induces large amounts of Ca 2+ to be rapidly released from calcium pools, disrupting the ER calcium balance and resulting in severe [Ca 2+ ] i dysregulation .…”

Section: Introductionmentioning

confidence: 99%

1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic Acid Acetoxymethyl Ester Loaded Reactive Oxygen Species Responsive Hyaluronic Acid–Bilirubin Nanoparticles for Acute Kidney Injury Therapy via Alleviating Calcium Overload Mediated Endoplasmic Reticulum Stress

Wang

Yan

et al. 2022

ACS Nano

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Calcium overload is one of the early determinants of the core cellular events that contribute to the pathogenesis of acute kidney injury (AKI), which include oxidative stress, ATP depletion, calcium overload, and inflammatory response with self-amplifying and interactive feedback loops that ultimately lead to cellular injury and renal failure. Excluding adjuvant therapy, there are currently no approved pharmacotherapies for the treatment of AKI. Using an adipic dihydride linker, we modified the hyaluronic acid polymer chain with a potent antioxidant, bilirubin, to produce an amphiphilic conjugate. Subsequently, we developed a kidney-targeted and reactive oxygen species (ROS)-responsive drug delivery system based on the flash nanocomplexation method to deliver a well-known intracellular calcium chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM, BA), with the goal of rescuing renal cell damage via rapidly scavenging of intracellularly overloaded Ca 2+ . In the ischemia−reperfusion (I/R) induced AKI rat model, a single dose of as-prepared formulation (BA 100 μg•kg −1 ) 6 h post-reperfusion significantly reduced renal function indicators by more than 60% within 12 h, significantly alleviated tissular pathological changes, ameliorated tissular oxidative damage, significantly inhibited apoptosis of renal tubular cells and the expression of renal tubular marker kidney injury molecule 1, etc., thus greatly reducing the risk of kidney failure. Mechanistically, the treatment with BA-loaded NPs significantly inhibited the activation of the ER stress cascade response (IRE1-TRAF2-JNK, ATF4-CHOP, and ATF6 axis) and regulated the downstream apoptosisrelated pathway while also reducing the inflammatory response. The BA-loaded NPs hold great promise as a potential therapy for I/R injury-related diseases. continued...

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Renal Nano-drug delivery for acute kidney Injury: Current status and future perspectives

Cited by 40 publications

References 174 publications

Dual-Responsive Curcumin-Loaded Nanoparticles for the Treatment of Cisplatin-Induced Acute Kidney Injury

Dual-Responsive Curcumin-Loaded Nanoparticles for the Treatment of Cisplatin-Induced Acute Kidney Injury

Nanodrugs alleviate acute kidney injury: Manipulate RONS at kidney

1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic Acid Acetoxymethyl Ester Loaded Reactive Oxygen Species Responsive Hyaluronic Acid–Bilirubin Nanoparticles for Acute Kidney Injury Therapy via Alleviating Calcium Overload Mediated Endoplasmic Reticulum Stress

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