Pannexin 1 mediates ferroptosis that contributes to renal ischemia/reperfusion injury

Su, L. Joseph; Jiang, Xiaofang; Yang, Cheng‐Ta; Zhang, Jiahao; Chen, Bo; Li, Yiming; Yao, Shijie; Xie, Qin; Gómez, Hernando; Murugan, Raghavan; Peng, Zhiyong

doi:10.1074/jbc.ra119.010949

Cited by 161 publications

(118 citation statements)

References 46 publications

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“…Numerous studies used TUNEL-positivity as a universal measure of DNA fragmentation-associated cell death in other types of cell death apart from apoptosis. For example, ferroptosis, a newly discovered form of programmed, non-apoptotic cell death triggered by oxidative damage that occurs during renal ischemia-reperfusion (IR) in mice, can be detected by TUNEL [ 26 ]. Pyroptosis, which is an inflammatory form of programmed cell death that is distinct from apoptosis and necrosis, is shown to be associated with TUNEL-positive signals [ 27 , 28 ].…”

Section: Tunel Principlesmentioning

confidence: 99%

TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation

Moore

Savenka

Basnakian

2021

IJMS

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Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay is a long-established assay used to detect cell death-associated DNA fragmentation (3’-OH DNA termini) by endonucleases. Because these enzymes are particularly active in the kidney, TUNEL is widely used to identify and quantify DNA fragmentation and cell death in cultured kidney cells and animal and human kidneys resulting from toxic or hypoxic injury. The early characterization of TUNEL as an apoptotic assay has led to numerous misinterpretations of the mechanisms of kidney cell injury. Nevertheless, TUNEL is becoming increasingly popular for kidney injury assessment because it can be used universally in cultured and tissue cells and for all mechanisms of cell death. Furthermore, it is sensitive, accurate, quantitative, easily linked to particular cells or tissue compartments, and can be combined with immunohistochemistry to allow reliable identification of cell types or likely mechanisms of cell death. Traditionally, TUNEL analysis has been limited to the presence or absence of a TUNEL signal. However, additional information on the mechanism of cell death can be obtained from the analysis of TUNEL patterns.

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Section: Tunel Principlesmentioning

confidence: 99%

TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation

Moore

Savenka

Basnakian

2021

IJMS

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“…The biochemical mechanism underlying ferroptosis is the iron-catalyzed formation of lipid radicals combined with glutathione (GSH) depletion or the inactivation of the lipid repair enzyme GSH peroxidase 4 (GPx4) [ 13 , 14 ]. Ferroptosis can be prevented by lipophilic antioxidants (e.g., CoQ10, vitamin E, ferrostatins, and liproxstatins) [ 15 ]. The small-molecule, ferrostatin-1 has been identified as a specific inhibitor of ferroptosis [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Nrf2 and STAT3 Alleviates Ferroptosis-Mediated IIR-ALI by Regulating SLC7A11

Qiang

Dong

Xia

et al. 2020

Oxidative Medicine and Cellular Longevity

153

101

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Acute lung injury (ALI) has gained increased attention in the field of critical illness research and is associated with a fatality rate of approximately 50%. Nuclear factor erythroid 2-related factor2 (Nrf2) is a key regulator of intracellular oxidation homeostasis and also functions as an antioxidant. It has been reported that Nrf2 associated antioxidant stress is closely related to ferroptosis inhibition. Signal transducer and activator of transcription 3 (STAT3) is activated into phosphorylated STAT3 (pSTAT3) in response to tissue damage and serves as a warning signal to enhance the inflammatory response. In this study, an intestinal ischemia/reperfusion-induced acute lung injury (IIR-ALI) model was established in C57BL/6 mice to investigate the role of Nrf2 in regulating IIR-ALI-associated ferroptosis. Compared with those in the IIR-ALI group, the injection of Fe (15 mg/kg) or ferrostatin-1 (5 mg/kg) (ferroptosis promoter and inhibitor, respectively) via the tail vein could aggravate or alleviate lung injury and pulmonary edema, respectively. Nrf2 was increased in IIR-ALI and promoted the phosphorylation of STAT3 to amplify downstream signals. An in vitro oxygen-glucose deprivation and reoxygenation (OGD-R) model was established in MLE12 cells to imitate the ischemia/reperfusion condition. The cells were transfected with lentiviruses to increase or downregulate the levels of STAT3. We found that Nrf2 and STAT3 played key roles in ferroptosis by regulating SLC7A11, which improved the pathological processes associated with ALI.

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“…Ferroptosis has been shown to induce the elimination of nerve cells in Parkinson’s disease 19 . In addition, in acute kidney injury, ferroptosis participated in the death of renal tubular epithelial cells 20 . Therefore, use of ferroptosis inducers may generate complications.…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between noncoding RNAs and ferroptosis: new dawn for overcoming cancer progression

Zhang

Wang

et al. 2020

Cell Death Dis

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Cancer progression including proliferation, metastasis, and chemoresistance has become a serious hindrance to cancer therapy. This phenomenon mainly derives from the innate insensitive or acquired resistance of cancer cells to apoptosis. Ferroptosis is a newly discovered mechanism of programmed cell death characterized by peroxidation of the lipid membrane induced by reactive oxygen species. Ferroptosis has been confirmed to eliminate cancer cells in an apoptosis-independent manner, however, the specific regulatory mechanism of ferroptosis is still unknown. The use of ferroptosis for overcoming cancer progression is limited. Noncoding RNAs have been found to play an important roles in cancer. They regulate gene expression to affect biological processes of cancer cells such as proliferation, cell cycle, and cell death. Thus far, the functions of ncRNAs in ferroptosis of cancer cells have been examined, and the specific mechanisms by which noncoding RNAs regulate ferroptosis have been partially discovered. However, there is no summary of ferroptosis associated noncoding RNAs and their functions in different cancer types. In this review, we discuss the roles of ferroptosis-associated noncoding RNAs in detail. Moreover, future work regarding the interaction between noncoding RNAs and ferroptosis is proposed, the possible obstacles are predicted and associated solutions are put forward. This review will deepen our understanding of the relationship between noncoding RNAs and ferroptosis, and provide new insights in targeting noncoding RNAs in ferroptosis associated therapeutic strategies.

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Pannexin 1 mediates ferroptosis that contributes to renal ischemia/reperfusion injury

Cited by 161 publications

References 46 publications

TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation

TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation

Nrf2 and STAT3 Alleviates Ferroptosis-Mediated IIR-ALI by Regulating SLC7A11

Crosstalk between noncoding RNAs and ferroptosis: new dawn for overcoming cancer progression

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