In vivo evidence for therapeutic applications of beclin 1 to promote recovery and inhibit fibrosis after acute kidney injury

Shi, Mingjun; Maique, Jenny; Shepard, Sierra; Seli, Olivia; Moe, Orson W.; Hu, Ming

doi:10.1016/j.kint.2021.09.030

Cited by 23 publications

(17 citation statements)

References 54 publications

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“…In the IRI model, more autophagic flux was seen in Becn1fA ‐deficient mice compared to wild‐type mice. This study confirmed that Beclin‐1 activity attenuates interstitial fibrosis and thus AKI‐to‐CKD transition (Shi et al, 2022).…”

Section: Autophagy In Aki‐to‐ckd Transitionsupporting

confidence: 86%

“…The role of autophagy in AKI and CKD is well defined. However, to further explore the role of autophagy in AKI‐to‐CKD transition, Shi et al (2022) demonstrated the protective role of beclin‐1 in different animal models, including cisplatin‐induced nephrotoxicity, unilateral ureteral obstruction, and bilateral IRI in rats. In the IRI model, more autophagic flux was seen in Becn1fA ‐deficient mice compared to wild‐type mice.…”

Section: Autophagy In Aki‐to‐ckd Transitionmentioning

confidence: 99%

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Role of endoplasmic reticulum stress and autophagy in the transition from acute kidney injury to chronic kidney disease

Habshi

Shelke

Kale

et al. 2022

Journal Cellular Physiology

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Acute kidney injury (AKI) and chronic kidney disease (CKD) are global health concerns with increasing rates in morbidity and mortality. Transition from AKI-to-CKD is common and requires awareness in the management of AKI survivors. AKIto-CKD transition is a main risk factor for the development of cardiovascular disease and progression to end-stage kidney disease. The mechanisms driving AKI-to-CKD transition are being explored to identify potential molecular and cellular targets for renoprotective drug interventions. Endoplasmic reticulum (ER) stress and autophagy are involved in the process of AKI-to-CKD transition. Excessive ER stress results in the persistent activation of unfolded protein response, which is an underneath cause of kidney cell death. Moreover, ER stress modulates autophagy and vice-versa.Autophagy is a degradation defensive mechanism protecting cells from malfunction.However, the underlying pathological mechanism involved in this interplay in the context of AKI-to-CKD transition is still unclear. In this review, we discuss the crosstalk between ER stress and autophagy in AKI, AKI-to-CKD transition, and CKD progression. In addition, we explore possible therapeutic targets that can regulate ER stress and autophagy to prevent AKI-to-CKD transition to improve the long-term prognosis of AKI survivors.

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Section: Autophagy In Aki‐to‐ckd Transitionsupporting

confidence: 86%

Section: Autophagy In Aki‐to‐ckd Transitionmentioning

confidence: 99%

Role of endoplasmic reticulum stress and autophagy in the transition from acute kidney injury to chronic kidney disease

Habshi

Shelke

Kale

et al. 2022

Journal Cellular Physiology

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“…Notably, the latest nephrotoxicity studies have commonly focused on the renoprotective mechanism, early warning, and nanomedicine of nephrotoxicity. Beclin-1, MiR-155, farnesoid X receptor, and mitochondrial homeostasis proteins may be novel therapy target strategies of nephrotoxicity through autophagy blockade, ferroptosis, and OS ( Kim et al, 2022 ; Shi et al, 2022 ; Yin et al, 2022 ; Zhang et al, 2022 ). In addition, phosphatidylcholines and taurine may be early biomarkers of nephrotoxicity using metabolomics and mass spectrometry imaging approaches ( Chen et al, 2022 ; Locci et al, 2022 ), while nuclear factor erythroid 2-related factor 2 (Nrf2) could predict the severity of nephrotoxicity using deep learning approach ( Feng et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Bibliometric and visual analysis of nephrotoxicity research worldwide

Duan

et al. 2022

Front. Pharmacol.

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Background: Nephrotoxicity of drugs contributes to acute kidney injury with high mortality and morbidity, which crucially limits the application and development of drugs. Although many publications on nephrotoxicity have been conducted globally, there needs to be a scientometric study to systematically analyze the intellectual landscape and frontiers research trends in the future.Methods: Publications on nephrotoxicity from 2011 to 2021 were collected to perform bibliometric visualization using VOSviewer, CiteSpace, and Scimago Graphica software based on the Web of Science Core Collection.Results: A total of 9,342 documents were analyzed, which were primarily published in the United States (1,861), China (1,724), and Egypt (701). For institutions, King Saud University (166) had the most publications; Food and Chemical Toxicology, PLOS One, and Antimicrobial Agents and Chemotherapy were productive journals, primarily concentrating on the mechanisms of nephrotoxicity and renoprotective in cisplatin and antibiotics, especially in oxidative stress. Burst detection suggested that cisplatin, piperacillin-tazobactam, vancomycin-induced nephrotoxicity, antioxidants, and new biomaterials are frontiers of research.Conclusion: This study first provides an updated perspective on nephrotoxicity and renoprotective strategies and mechanisms. This perspective may benefit researchers in choosing suitable journals and collaborators and assisting them in the deep understanding of the nephrotoxicity and renoprotective hotspots and frontiers.

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“…Similarly in the experimental model of CP-induced CKD, the natural flavonoid, farrerol upregulated mitochondrial autophagy, thereby inhibiting inflammation and renal fibrosis induced by CP and closely contributing to CKD (Ma et al, 2021). Along the same line, Shi et al (2022) recently demonstrated that deficiency of beclin-1, the key molecule of autophagy, promoted renal fibrosis and consequently delayed recovery following renal injury.…”

Section: The Potential Mechanisms Underlying Autophagy Protectionmentioning

confidence: 94%

Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential

Alassaf

Attia

2023

Front. Pharmacol.

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Cisplatin (CP) is a broad-spectrum antineoplastic agent, used to treat many different types of malignancies due to its high efficacy and low cost. However, its use is largely limited by acute kidney injury (AKI), which, if left untreated, may progress to cause irreversible chronic renal dysfunction. Despite substantial research, the exact mechanisms of CP-induced AKI are still so far unclear and effective therapies are lacking and desperately needed. In recent years, necroptosis, a novel subtype of regulated necrosis, and autophagy, a form of homeostatic housekeeping mechanism have witnessed a burgeoning interest owing to their potential to regulate and alleviate CP-induced AKI. In this review, we elucidate in detail the molecular mechanisms and potential roles of both autophagy and necroptosis in CP-induced AKI. We also explore the potential of targeting these pathways to overcome CP-induced AKI according to recent advances.

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In vivo evidence for therapeutic applications of beclin 1 to promote recovery and inhibit fibrosis after acute kidney injury

Cited by 23 publications

References 54 publications

Role of endoplasmic reticulum stress and autophagy in the transition from acute kidney injury to chronic kidney disease

Role of endoplasmic reticulum stress and autophagy in the transition from acute kidney injury to chronic kidney disease

Bibliometric and visual analysis of nephrotoxicity research worldwide

Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential

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