Biochemical and Biophysical Research Communications

Journal Information
ISSN / EISSN : 0006291X / 10902104
Current Publisher: Elsevier BV (10.1016)
Former Publisher: Elsevier BV (10.1006)
Total articles ≅ 87,413
Google Scholar h5-index: 64
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Latest articles in this journal

Ming Fang, Le Kang, Xiaolang Wang, Xianan Guo, Weidong Wang, Biaojie Qin, Xiangning Du, Qingzhu Tang, Hongli Lin
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.037

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Lingdan Chen, Wenjun He, Bin Peng, Mingjie Yuan, Neng Wang, Jian Wang, Wenju Lu, Tao Wang
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.09.106

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Yansheng Feng, Ngonidzashe B. Madungwe, Abdulhafiz D. Imam Aliagan, Nathalie Tombo, Jean C. Bopassa
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.006

Abstract:Ferroptosis is a distinct iron-dependent mechanism of regulated cell death recognized in cancer and ischemia/reperfusion (I/R) injury of different organs. It has been reported that molecules such as liproxstatin-1 (Lip-1) inhibit ferroptosis and promote cell survival however, the mechanisms underlying this action are not clearly understood. We investigated the role and mechanism of Lip-1 in reducing cell death in the ischemic myocardium. Using an I/R model of isolated perfused mice hearts in which Lip-1 was given at the onset of reperfusion, we found that Lip-1 protects the heart by reducing myocardial infarct sizes and maintaining mitochondrial structural integrity and function. Further investigation revealed that Lip-1-induced cardioprotection is mediated by a reduction of VDAC1 levels and oligomerization, but not VDAC2/3. Lip-1 treatment also decreased mitochondrial reactive oxygen species production and rescued the reduction of the antioxidant GPX4 caused by I/R stress. Meanwhile, mitochondrial Ca2+ retention capacity needed to induce mitochondrial permeability transition pore opening did not change with Lip-1 treatment. Thus, we report that Lip-1 induces cardioprotective effects against I/R injury by reducing VDAC1 levels and restoring GPX4 levels.
Masahiko Kume, Hirohisa Chiyoda, Kenji Kontani, Toshiaki Katada, Masamitsu Fukuyama
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.045

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Meijuan Geng, Yiyi Yang, Xinyi Cao, Lin Dang, Tianye Zhang, Lirong Zhang
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.052

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Gang Jin, Yanjin Su, Qianlan Dong, Xiaohong Zhao, Linping Zhang, Xiaohui Yan
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.09.130

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Hyoji Kim, Ati Burassakarn, Yuting Kang, Hisashi Iizasa, Hironori Yoshiyama
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.028

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Hai Wu, Minjun Li, Chao Peng, Yue Yin, Haojie Guo, Weiwei Wang, Qin Xu, Huan Zhou, Chunyan Xu, Feng Yu, et al.
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.063

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Feifei Hu, Youyou Lin, Yidan Zuo, Ruyi Chen, Shengnan Luo, Zhen Su
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.047

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Kenta Niimi, Yumi Adachi, Hiroko Ishikawa, Wataru Yamaguchi, Yoshiaki Kubota, Shinobu Inagaki, Tatsuo Furuyama
Biochemical and Biophysical Research Communications; doi:10.1016/j.bbrc.2019.10.040

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