Mitochondrial 4-HNE derived from MAO-A promotes mitoCa2+ overload in chronic postischemic cardiac remodeling-Reference-Cited by-同舟云学术

Mitochondrial 4-HNE derived from MAO-A promotes mitoCa2+ overload in chronic postischemic cardiac remodeling

Published:2019-12-09 Issue:6 Volume:27 Page:1907-1923
ISSN:1350-9047
Container-title:Cell Death & Differentiation
language:en
Short-container-title:Cell Death Differ

Author:

Santin Yohan,Fazal Loubina,Sainte-Marie Yannis,Sicard Pierre,Maggiorani Damien,Tortosa Florence,Yücel Yasemin Yücel,Teyssedre Lise,Rouquette Jacques,Marcellin Marlene,Vindis Cécile,Shih Jean C.,Lairez Olivier,Burlet-Schiltz Odile,Parini Angelo,Lezoualc’h Frank,Mialet-Perez Jeanne^ORCID

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Molecular Biology

Link

http://www.nature.com/articles/s41418-019-0470-y.pdf

Reference36 articles.

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3. Bertero E, Maack C. Calcium signaling and reactive oxygen species in mitochondria. Circulation Res. 2018;122:1460–78.

4. Luongo TS, Lambert JP, Gross P, Nwokedi M, Lombardi AA, Shanmughapriya S, et al. The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability. Nature. 2017;545:93–7.

5. Santulli G, Xie WJ, Reiken SR, Marks AR. Mitochondrial calcium overload is a key determinant in heart failure. Proc Natl Acad Sci USA. 2015;112:11389–94.

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