Hypoxia-induced interaction of filamin with Drp1 causes mitochondrial hyperfission–associated myocardial senescence-Reference-Cited by-同舟云学术

Hypoxia-induced interaction of filamin with Drp1 causes mitochondrial hyperfission–associated myocardial senescence

Published:2018-11-13 Issue:556 Volume:11 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Nishimura Akiyuki¹²³⁴,Shimauchi Tsukasa¹²⁵,Tanaka Tomohiro¹²^ORCID,Shimoda Kakeru¹²³,Toyama Takashi¹⁴⁶,Kitajima Naoyuki¹⁴,Ishikawa Tatsuya⁴⁷,Shindo Naoya⁴,Numaga-Tomita Takuro¹²³,Yasuda Satoshi⁸,Sato Yoji⁴⁸,Kuwahara Koichiro⁹^ORCID,Kumagai Yoshito⁶,Akaike Takaaki¹⁰,Ide Tomomi⁵,Ojida Akio⁴,Mori Yasuo¹¹,Nishida Motohiro¹²³⁴^ORCID

Affiliation:

1. National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Aichi 444-8787, Japan.

2. Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Aichi 444-8787, Japan.

3. SOKENDAI (School of Life Science, The Graduate University for Advanced Studies), Aichi 444-8787, Japan.

4. Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.

5. Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.

6. Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.

7. EA Pharma Co. Inc., Tokyo 104-0042, Japan.

8. National Institute of Health Sciences, Kanagawa 210-9501, Japan.

9. Shinshu University School of Medicine, Nagano 390-8621, Japan.

10. Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.

11. Graduate School of Engineering, Kyoto University, Kyoto 615-8510, Japan.

Abstract

Filamin enhances Drp1-mediated mitochondrial fission and cellular senescence after myocardial infarction.

Funder

JST PRESTO

JSPS KAKENHI

Ministry of Education, Culture, Sports, Science and Technology

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference65 articles.

1. Mitoconfusion: Noncanonical Functioning of Dynamism Factors in Static Mitochondria of the Heart

2. Mitochondrial fission/fusion and cardiomyopathy

3. Mitochondrial fusion and fission proteins as novel therapeutic targets for treating cardiovascular disease

4. Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

5. Mitochondrial Fission and Fusion Factors Reciprocally Orchestrate Mitophagic Culling in Mouse Hearts and Cultured Fibroblasts

Cited by 102 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Inorganic sulfides prevent osimertinib-induced mitochondrial dysfunction in human iPS cell-derived cardiomyocytes;Journal of Pharmacological Sciences;2024-10

2. Mitochondrial unfolded protein response mechanism and its cardiovascular protective effects;Biomedicine & Pharmacotherapy;2024-08

3. Supersulfide catabolism participates in maladaptive remodeling of cardiac cells;Journal of Pharmacological Sciences;2024-08

4. Recent advances of PIWI‐interacting RNA in cardiovascular diseases;Clinical and Translational Medicine;2024-07-31

5. Anti-atrial Fibrillatory and Cardiorenal Protective Effects of the Combination of Valsartan and Cilnidipine in Dahl Salt-Sensitive Rats;Biological and Pharmaceutical Bulletin;2024-07-30