CO‐Releasing Molecule‐2 Prevents Acute Kidney Injury through Suppression of ROS‐Fyn‐ER Stress Signaling in Mouse Model

Uddin, Jamal; Jeong, Jeewon; Pak, Eun Seon; Ha, Hunjoo

doi:10.1155/2021/9947772

Cited by 14 publications

(10 citation statements)

References 63 publications

(102 reference statements)

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“…Mitochondrial dysfunction is closely related to variations in the intracellular and extracellular environments. During the process of sepsis, renal microcirculation and inflammatory insults lead to abnormalities of mitochondria in both vascular ECs and TECs, causing the damage of renal cells (Figure 2) (137)(138)(139).…”

Section: Mitochondria and Oxidative Stress/nitrosative Stressmentioning

confidence: 99%

“…After the production of excess ROS, cells develop a status of oxidative stress, resulting in the oxidatively modification of DNA, proteins and lipids. ROS also directly damages the structure of mitochondria and further aggravates its biosynthesis ( 137 , 138 ).…”

Section: Cellular Processes Interact With Programmed Cell Deathmentioning

confidence: 99%

“…Recently, Diaz-Quintana et al ( 155 ) reported that oxidative stress attacks cardiolipin, a lipid component on the outer membrane of the mitochondria, by oxidizing the lipids and uncoupling cyto c from cardiolipin to generate an oxidized form of cyto c. At the same time, due to the destruction of mitochondrial membrane lipids, cyto c is released into the cytoplasm and activates the caspase family, causing cell apoptosis. It has also been reported that ROS activates Bax either through the JNK/p38 mitogen-activated protein kinase (MAPK) signaling pathway or directly by phosphorylation, and activated Bax forms dimers and translocates to the mitochondria ( 138 , 139 ). Additionally, ROS can cause apoptosis through activating p53 or Bim (Bcl-2 interacting mediator of cell death), inhibiting the mitochondrial protective protein Bcl-2, and further activating the Bax complex to form membrane pores outside the mitochondria, leading to the release of mitochondrial cyto c ( 154 ).…”

Section: Cellular Processes Interact With Programmed Cell Deathmentioning

confidence: 99%

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The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Wang

et al. 2021

Front. Med.

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Sepsis is a systemic inflammatory response syndrome caused by infection, following with acute injury to multiple organs. Sepsis-induced acute kidney injury (AKI) is currently recognized as one of the most severe complications related to sepsis. The pathophysiology of sepsis-AKI involves multiple cell types, including macrophages, vascular endothelial cells (ECs) and renal tubular epithelial cells (TECs), etc. More significantly, programmed cell death including apoptosis, necroptosis and pyroptosis could be triggered by sepsis in these types of cells, which enhances AKI progress. Moreover, the cross-talk and connections between these cells and cell death are critical for better understanding the pathophysiological basis of sepsis-AKI. Mitochondria dysfunction and oxidative stress are traditionally considered as the leading triggers of programmed cell death. Recent findings also highlight that autophagy, mitochondria quality control and epigenetic modification, which interact with programmed cell death, participate in the damage process in sepsis-AKI. The insightful understanding of the programmed cell death in sepsis-AKI could facilitate the development of effective treatment, as well as preventive methods.

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Section: Mitochondria and Oxidative Stress/nitrosative Stressmentioning

confidence: 99%

Section: Cellular Processes Interact With Programmed Cell Deathmentioning

confidence: 99%

Section: Cellular Processes Interact With Programmed Cell Deathmentioning

confidence: 99%

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The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Wang

et al. 2021

Front. Med.

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“…Renal inflammation is initiated by several factors including immune-mediated inflammatory mediators and a subsequent renal dysfunction or nephrotoxicity (Figure 3) [45][46][47][48][49]. Moreover, increased uric acid triggers renal inflammation through the c-Jun N-terminal kinases (JNK) signaling pathway and nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)-and pyrin domain-containing protein (NLRP) 3 inflammasome.…”

Section: Effects Of Mangiferin On Renal Inflammationmentioning

confidence: 99%

Renoprotective Effects of Mangiferin: Pharmacological Advances and Future Perspectives

Akter¹,

Moni²,

Faisal

et al. 2022

IJERPH

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Both acute and chronic kidney diseases substantially contribute to the morbidities and mortality of patients worldwide. The existing therapeutics, which are mostly developed from synthetic sources, present some unexpected effects in patients, provoking researchers to explore potential novel alternatives. Natural products that have protective effects against various renal pathologies could be potential drug candidates for kidney diseases. Mangiferin is a natural polyphenol predominantly isolated from Mangifera indica and possesses multiple health benefits against various human ailments, including kidney disease. The main objective of this review is to update the renoprotective potentials of mangiferin with underlying molecular pharmacology and to highlight the recent development of mangiferin-based therapeutics toward kidney problems. Literature published over the past decade suggests that treatment with mangiferin attenuates renal inflammation and oxidative stress, improves interstitial fibrosis and renal dysfunction, and ameliorates structural alteration in the kidney. Therefore, mangiferin could be used as a multi-target therapeutic candidate to treat renal diseases. Although mangiferin-loaded nanoparticles have shown therapeutic promise against various human diseases, there is limited information on the targeted delivery of mangiferin in the kidney. Further research is required to gain insight into the molecular pharmacology of mangiferin targeting kidney diseases and translate the preclinical results into clinical use.

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“…The kidney is responsible for maintaining whole-body homeostasis. Kidney disease is characterized by inflammation as a major pathology [58][59][60]. Acute or chronic disease such as ischemia, toxins, or inflammation affects kidney tubules, causing kidney fibrosis that is associated with reduction of GFR in kidneys [61].…”

Section: Inflammationmentioning

confidence: 99%

Prospects for Protective Potential of Moringa oleifera against Kidney Diseases

Akter¹,

Rahman²,

Moni³

et al. 2021

Plants

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Kidney diseases are regarded as one of the major public health issues in the world. The objectives of this study were: (i) to investigate the causative factors involved in kidney disease and the therapeutic aspects of Moringa oleifera, as well as (ii) the effectiveness of M. oleifera in the anti-inflammation and antioxidant processes of the kidney while minimizing all potential side effects. In addition, we proposed a hypothesis to improve M. oleifera based drug development. This study was updated by searching the key words M. oleifera on kidney diseases and M. oleifera on oxidative stress, inflammation, and fibrosis in online research databases such as PubMed and Google Scholar. The following validation checking and scrutiny analysis of the recently published articles were used to explore this study. The recent existing research has found that M. oleifera has a plethora of health benefits. Individual medicinal properties of M. oleifera leaf extract, seed powder, stem extract, and the whole extract (ethanol/methanol) can up-increase the activity of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), while decreasing the activity of inflammatory cytokines such as TNF-α, IL-1β, IL-6, and COX-2. In our study, we have investigated the properties of this plant against kidney diseases based on existing knowledge with an updated review of literature. Considering the effectiveness of M. oleifera, this study would be useful for further research into the pharmacological potential and therapeutic insights of M. oleifera, as well as prospects of Moringa-based effective medicine development for human benefits.

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CO‐Releasing Molecule‐2 Prevents Acute Kidney Injury through Suppression of ROS‐Fyn‐ER Stress Signaling in Mouse Model

Cited by 14 publications

References 63 publications

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Renoprotective Effects of Mangiferin: Pharmacological Advances and Future Perspectives

Prospects for Protective Potential of Moringa oleifera against Kidney Diseases

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