TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis

Xiucui Ma; David R. Rawnsley; Attila Kovacs; Moydul Islam; John T. Murphy; Chen Zhao; Minu Kumari; Layla Foroughi; Haiyan Liu; Kevin Qi; Aaradhya Diwan; Krzysztof Hyrc; Sarah Evans; Takashi Satoh; Brent A. French; Kenneth B. Margulies; Ali Javaheri; Babak Razani; Douglas Mann; Kartik Mani; Abhinav Diwan

doi:10.1016/j.jacbts.2021.12.002

TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis

Xiucui Ma, David R. Rawnsley, Attila Kovacs, Moydul Islam, John T. Murphy, Chen Zhao, Minu Kumari, Layla Foroughi, Haiyan Liu, Kevin Qi, Aaradhya Diwan, Krzysztof Hyrc, Sarah Evans, Takashi Satoh, Brent A. French, Kenneth B. Margulies, Ali Javaheri, Babak Razani, Douglas Mann, Kartik ManiAbhinav Diwan

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

Mitochondria are essential for cardiac myocyte function, but damaged mitochondria trigger cardiac myocyte death. Although mitophagy, a lysosomal degradative pathway to remove damaged mitochondria, is robustly active in cardiac myocytes in the unstressed heart, its mechanisms and physiological role remain poorly defined. We discovered a critical role for TRAF2, an innate immunity effector protein with E3 ubiquitin ligase activity, in facilitating physiological cardiac myocyte mitophagy in the adult heart, to prevent inflammation and cell death, and maintain myocardial homeostasis.

Original language	English
Pages (from-to)	223-243
Number of pages	21
Journal	JACC: Basic to Translational Science
Volume	7
Issue number	3
DOIs	https://doi.org/10.1016/j.jacbts.2021.12.002
State	Published - Mar 2022

Keywords

TRAF2
cell death
inflammation
mitophagy

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10.1016/j.jacbts.2021.12.002

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Ma, X., Rawnsley, D. R., Kovacs, A., Islam, M., Murphy, J. T., Zhao, C., Kumari, M., Foroughi, L., Liu, H., Qi, K., Diwan, A., Hyrc, K., Evans, S., Satoh, T., French, B. A., Margulies, K. B., Javaheri, A., Razani, B., Mann, D., ... Diwan, A. (2022). TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis. JACC: Basic to Translational Science, 7(3), 223-243. https://doi.org/10.1016/j.jacbts.2021.12.002

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title = "TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis",

abstract = "Mitochondria are essential for cardiac myocyte function, but damaged mitochondria trigger cardiac myocyte death. Although mitophagy, a lysosomal degradative pathway to remove damaged mitochondria, is robustly active in cardiac myocytes in the unstressed heart, its mechanisms and physiological role remain poorly defined. We discovered a critical role for TRAF2, an innate immunity effector protein with E3 ubiquitin ligase activity, in facilitating physiological cardiac myocyte mitophagy in the adult heart, to prevent inflammation and cell death, and maintain myocardial homeostasis.",

keywords = "TRAF2, cell death, inflammation, mitophagy",

author = "Xiucui Ma and Rawnsley, {David R.} and Attila Kovacs and Moydul Islam and Murphy, {John T.} and Chen Zhao and Minu Kumari and Layla Foroughi and Haiyan Liu and Kevin Qi and Aaradhya Diwan and Krzysztof Hyrc and Sarah Evans and Takashi Satoh and French, {Brent A.} and Margulies, {Kenneth B.} and Ali Javaheri and Babak Razani and Douglas Mann and Kartik Mani and Abhinav Diwan",

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year = "2022",

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doi = "10.1016/j.jacbts.2021.12.002",

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Ma, X , Rawnsley, DR, Kovacs, A, Islam, M, Murphy, JT, Zhao, C, Kumari, M, Foroughi, L, Liu, H, Qi, K, Diwan, A, Hyrc, K, Evans, S, Satoh, T, French, BA, Margulies, KB, Javaheri, A, Razani, B, Mann, D, Mani, K & Diwan, A 2022, 'TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis', JACC: Basic to Translational Science, vol. 7, no. 3, pp. 223-243. https://doi.org/10.1016/j.jacbts.2021.12.002

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T1 - TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis

AU - Ma, Xiucui

AU - Rawnsley, David R.

AU - Kovacs, Attila

AU - Islam, Moydul

AU - Murphy, John T.

AU - Zhao, Chen

AU - Kumari, Minu

AU - Foroughi, Layla

AU - Liu, Haiyan

AU - Qi, Kevin

AU - Diwan, Aaradhya

AU - Hyrc, Krzysztof

AU - Evans, Sarah

AU - Satoh, Takashi

AU - French, Brent A.

AU - Margulies, Kenneth B.

AU - Javaheri, Ali

AU - Razani, Babak

AU - Mann, Douglas

AU - Mani, Kartik

AU - Diwan, Abhinav

PY - 2022/3

Y1 - 2022/3

N2 - Mitochondria are essential for cardiac myocyte function, but damaged mitochondria trigger cardiac myocyte death. Although mitophagy, a lysosomal degradative pathway to remove damaged mitochondria, is robustly active in cardiac myocytes in the unstressed heart, its mechanisms and physiological role remain poorly defined. We discovered a critical role for TRAF2, an innate immunity effector protein with E3 ubiquitin ligase activity, in facilitating physiological cardiac myocyte mitophagy in the adult heart, to prevent inflammation and cell death, and maintain myocardial homeostasis.

AB - Mitochondria are essential for cardiac myocyte function, but damaged mitochondria trigger cardiac myocyte death. Although mitophagy, a lysosomal degradative pathway to remove damaged mitochondria, is robustly active in cardiac myocytes in the unstressed heart, its mechanisms and physiological role remain poorly defined. We discovered a critical role for TRAF2, an innate immunity effector protein with E3 ubiquitin ligase activity, in facilitating physiological cardiac myocyte mitophagy in the adult heart, to prevent inflammation and cell death, and maintain myocardial homeostasis.

KW - TRAF2

KW - cell death

KW - inflammation

KW - mitophagy

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AN - SCOPUS:85122532495

SN - 2452-302X

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TRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis

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