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Article ; Online: The nexus between redox state and intermediary metabolism.

Zoccarato, Anna / Nabeebaccus, Adam A / Oexner, Rafael R / Santos, Celio X C / Shah, Ajay M

2021 Volume 289, Issue 18, Page(s) 5440–5462

Abstract: Reactive oxygen species (ROS) are not just a by-product of cellular metabolic processes but act as signalling molecules that regulate both physiological and pathophysiological processes. A close connection exists in cells between redox homeostasis and ... ...

Abstract	Reactive oxygen species (ROS) are not just a by-product of cellular metabolic processes but act as signalling molecules that regulate both physiological and pathophysiological processes. A close connection exists in cells between redox homeostasis and cellular metabolism. In this review, we describe how intracellular redox state and glycolytic intermediary metabolism are closely coupled. On the one hand, ROS signalling can control glycolytic intermediary metabolism by direct regulation of the activity of key metabolic enzymes and indirect regulation via redox-sensitive transcription factors. On the other hand, metabolic adaptation and reprogramming in response to physiological or pathological stimuli regulate intracellular redox balance, through mechanisms such as the generation of reducing equivalents. We also discuss the impact of these intermediary metabolism-redox circuits in physiological and disease settings across different tissues. A better understanding of the mechanisms regulating these intermediary metabolism-redox circuits will be crucial to the development of novel therapeutic strategies.
MeSH term(s)	Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Signal Transduction/physiology ; Transcription Factors/metabolism
Chemical Substances	Reactive Oxygen Species ; Transcription Factors
Language	English
Publishing date	2021-09-20
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16191
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Article: The nexus between redox state and intermediary metabolism

Zoccarato, Anna / Nabeebaccus, Adam A. / Oexner, Rafael R. / Santos, Celio X. C. / Shah, Ajay M.

FEBS journal. 2022 Sept., v. 289, no. 18

2022

Abstract: Reactive oxygen species (ROS) are not just a by‐product of cellular metabolic processes but act as signalling molecules that regulate both physiological and pathophysiological processes. A close connection exists in cells between redox homeostasis and ... ...

Abstract	Reactive oxygen species (ROS) are not just a by‐product of cellular metabolic processes but act as signalling molecules that regulate both physiological and pathophysiological processes. A close connection exists in cells between redox homeostasis and cellular metabolism. In this review, we describe how intracellular redox state and glycolytic intermediary metabolism are closely coupled. On the one hand, ROS signalling can control glycolytic intermediary metabolism by direct regulation of the activity of key metabolic enzymes and indirect regulation via redox‐sensitive transcription factors. On the other hand, metabolic adaptation and reprogramming in response to physiological or pathological stimuli regulate intracellular redox balance, through mechanisms such as the generation of reducing equivalents. We also discuss the impact of these intermediary metabolism–redox circuits in physiological and disease settings across different tissues. A better understanding of the mechanisms regulating these intermediary metabolism–redox circuits will be crucial to the development of novel therapeutic strategies.
Keywords	byproducts ; glycolysis ; homeostasis ; reactive oxygen species ; therapeutics
Language	English
Dates of publication	2022-09
Size	p. 5440-5462.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16191
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Article ; Online: The regulation of cardiac intermediary metabolism by NADPH oxidases.

Nabeebaccus, Adam A / Reumiller, Christina M / Shen, Jie / Zoccarato, Anna / Santos, Celio X C / Shah, Ajay M

Cardiovascular research

2022 Volume 118, Issue 17, Page(s) 3305–3319

Abstract: NADPH oxidases (NOXs), enzymes whose primary function is to generate reactive oxygen species, are important regulators of the heart's physiological function and response to pathological insults. The role of NOX-driven redox signalling in ... ...

Abstract	NADPH oxidases (NOXs), enzymes whose primary function is to generate reactive oxygen species, are important regulators of the heart's physiological function and response to pathological insults. The role of NOX-driven redox signalling in pathophysiological myocardial remodelling, including processes such as interstitial fibrosis, contractile dysfunction, cellular hypertrophy, and cell survival, is well recognized. While the NOX2 isoform promotes many detrimental effects, the NOX4 isoform has attracted considerable attention as a driver of adaptive stress responses both during pathology and under physiological states such as exercise. Recent studies have begun to define some of the NOX4-modulated mechanisms that may underlie these adaptive responses. In particular, novel functions of NOX4 in driving cellular metabolic changes have emerged. Alterations in cellular metabolism are a recognized hallmark of the heart's response to physiological and pathological stresses. In this review, we highlight the emerging roles of NOX enzymes as important modulators of cellular intermediary metabolism in the heart, linking stress responses not only to myocardial energetics but also other functions. The novel interplay of NOX-modulated redox signalling pathways and intermediary metabolism in the heart is unravelling a new aspect of the fascinating biology of these enzymes which will inform a better understanding of how they drive adaptive responses. We also discuss the implications of these new findings for therapeutic approaches that target metabolism in cardiac disease.
MeSH term(s)	NADPH Oxidases/metabolism ; Myocardium/metabolism ; Reactive Oxygen Species/metabolism ; Heart ; Oxidative Stress ; Protein Isoforms/metabolism ; NADPH Oxidase 4/metabolism
Chemical Substances	NADPH Oxidases (EC 1.6.3.-) ; Reactive Oxygen Species ; Protein Isoforms ; NADPH Oxidase 4 (EC 1.6.3.-)
Language	English
Publishing date	2022-03-21
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvac030
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Article: NADPH Oxidase 2 Mediates Myocardial Oxygen Wasting in Obesity.

Hafstad, Anne D / Hansen, Synne S / Lund, Jim / Santos, Celio X C / Boardman, Neoma T / Shah, Ajay M / Aasum, Ellen

Antioxidants (Basel, Switzerland)

2020 Volume 9, Issue 2

Abstract: Obesity and diabetes are independent risk factors for cardiovascular diseases, and they are associated with the development of a specific cardiomyopathy with elevated myocardial oxygen consumption ( ... ...

Abstract	Obesity and diabetes are independent risk factors for cardiovascular diseases, and they are associated with the development of a specific cardiomyopathy with elevated myocardial oxygen consumption (MVO
Language	English
Publishing date	2020-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9020171
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Article ; Online: Nrf2 attenuates the innate immune response after experimental myocardial infarction.

Bromage, Daniel I / Trevelin, Silvia C / Huntington, Josef / Yang, Victoria X / Muthukumar, Ananya / Mackie, Sarah J / Sawyer, Greta / Zhang, Xiaohong / Santos, Celio X C / Safinia, Niloufar / Smyrnias, Ioannis / Giacca, Mauro / Ivetic, Aleksandar / Shah, Ajay M

Biochemical and biophysical research communications

2022 Volume 606, Page(s) 10–16

Abstract: Background: There is compelling evidence implicating dysregulated inflammation in the mechanism of ventricular remodeling and heart failure (HF) after MI. The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2, encoded by Nfe2l2) is a ... ...

Abstract	Background: There is compelling evidence implicating dysregulated inflammation in the mechanism of ventricular remodeling and heart failure (HF) after MI. The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2, encoded by Nfe2l2) is a promising target in this context since it impedes transcriptional upregulation of pro-inflammatory cytokines and is anti-inflammatory in various murine models. Objectives: We aimed to investigate the contribution of Nrf2 to the inflammatory response after experimental myocardial infarction (MI). Methods: We subjected Nrf2 Results: FACS analysis demonstrated a profoundly inflamed phenotype in the hearts of global Nrf2 Conclusions: Taken together, the results suggest that Nrf2 signalling in leukocytes, and possibly CCR2
MeSH term(s)	Animals ; Cytokines/metabolism ; Disease Models, Animal ; Immunity, Innate ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Ventricular Remodeling/physiology
Chemical Substances	Cytokines ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse
Language	English
Publishing date	2022-03-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.03.043
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Article ; Online: Human blood vessel organoids reveal a critical role for CTGF in maintaining microvascular integrity.

Nature communications

2023 Volume 14, Issue 1, Page(s) 5552

Abstract: The microvasculature plays a key role in tissue perfusion and exchange of gases and metabolites. In this study we use human blood vessel organoids (BVOs) as a model of the microvasculature. BVOs fully recapitulate key features of the human ... ...

Abstract	The microvasculature plays a key role in tissue perfusion and exchange of gases and metabolites. In this study we use human blood vessel organoids (BVOs) as a model of the microvasculature. BVOs fully recapitulate key features of the human microvasculature, including the reliance of mature endothelial cells on glycolytic metabolism, as concluded from metabolic flux assays and mass spectrometry-based metabolomics using stable tracing of
MeSH term(s)	Humans ; Biological Assay ; Endothelial Cells ; Microvessels ; Organoids ; Phosphoric Monoester Hydrolases ; Proteomics
Chemical Substances	Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; CCN2 protein, human
Language	English
Publishing date	2023-09-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41326-2
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Article ; Online: Redox signaling in the cardiomyocyte: From physiology to failure.

Santos, Celio X C / Raza, Sadaf / Shah, Ajay M

The international journal of biochemistry & cell biology

2016 Volume 74, Page(s) 145–151

Abstract: The specific effect of oxygen and reactive oxygen species (ROS) in mediating post-translational modification of protein targets has emerged as a key mechanism regulating signaling components, a process termed redox signaling. ROS act in the post- ... ...

Abstract	The specific effect of oxygen and reactive oxygen species (ROS) in mediating post-translational modification of protein targets has emerged as a key mechanism regulating signaling components, a process termed redox signaling. ROS act in the post-translational modification of multiple target proteins including receptors, kinases, phosphatases, ion channels and transcription factors. Both O2 and ROS are major source of electrons in redox reactions in aerobic organisms. Because the heart has the highest O2 consumption among body organs, it is not surprising that redox signaling is central to heart function and pathophysiology. In this article, we review some of the main cardiac redox signaling pathways and their roles in the cardiomyocyte and in heart failure, with particular focus on the specific molecular targets of ROS in the heart.
MeSH term(s)	Heart Failure/physiopathology ; Humans ; Myocytes, Cardiac/pathology ; Myocytes, Cardiac/physiology ; Oxidation-Reduction ; Protein Processing, Post-Translational ; Reactive Oxygen Species ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2016-03-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2016.03.002
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Article: Nrf2 attenuates the innate immune response after experimental myocardial infarction

Bromage, Daniel I. / Trevelin, Silvia C. / Huntington, Josef / Yang, Victoria X. / Muthukumar, Ananya / Mackie, Sarah J. / Sawyer, Greta / Zhang, Xiaohong / Santos, Celio X.C. / Safinia, Niloufar / Smyrnias, Ioannis / Giacca, Mauro / Ivetic, Aleksandar / Shah, Ajay M.

Biochemical and biophysical research communications. 2022 May 28, v. 606

2022

Abstract: There is compelling evidence implicating dysregulated inflammation in the mechanism of ventricular remodeling and heart failure (HF) after MI. The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2, encoded by Nfe2l2) is a promising ... ...

Abstract	There is compelling evidence implicating dysregulated inflammation in the mechanism of ventricular remodeling and heart failure (HF) after MI. The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2, encoded by Nfe2l2) is a promising target in this context since it impedes transcriptional upregulation of pro-inflammatory cytokines and is anti-inflammatory in various murine models. We aimed to investigate the contribution of Nrf2 to the inflammatory response after experimental myocardial infarction (MI). We subjected Nrf2⁻/⁻ mice and wild type (WT) controls to permanent left coronary artery (LCA) ligation. The inflammatory response was investigated with fluorescence-activated cell sorting (FACS) analysis of peripheral blood and heart cell suspensions, together with qRT-PCR of infarcted tissue for chemokines and their receptors. To investigate whether Nrf2-mediated transcription is a dedicated function of leukocytes, we interrogated publicly available RNA-sequencing (RNA-seq) data from mouse hearts after permanent LCA ligation for Nrf2-regulated gene (NRG) expression. FACS analysis demonstrated a profoundly inflamed phenotype in the hearts of global Nrf2⁻/⁻ mice as compared to WT mice after MI. Moreover, infarcted tissue from Nrf2⁻/⁻ mice displayed higher expression of mRNA coding for inflammatory cytokines, chemokines, and their receptors, including IL-6, Ccl2, and Cxcr4. RNA-seq analysis showed upregulated NRG expression in WT mice after MI compared to naive mice, which was significantly higher in bioinformatically isolated CCR2⁺ cells. Taken together, the results suggest that Nrf2 signalling in leukocytes, and possibly CCR2⁺ monocytes and monocyte-derived cardiac resident macrophages, may be potential targets to prevent post-MI ventricular remodeling.
Keywords	basic-leucine zipper transcription factors ; chemokines ; coronary vessels ; genes ; heart ; heart failure ; inflammation ; innate immunity ; interleukin-6 ; macrophages ; mice ; monocytes ; myocardial infarction ; phenotype ; research ; sequence analysis ; transcription (genetics)
Language	English
Dates of publication	2022-0528
Size	p. 10-16.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.03.043
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Article ; Online: Doxorubicin induces cardiotoxicity in a pluripotent stem cell model of aggressive B cell lymphoma cancer patients.

Basic research in cardiology

2022 Volume 117, Issue 1, Page(s) 13

Abstract: Cancer therapies with anthracyclines have been shown to induce cardiovascular complications. The aims of this study were to establish an in vitro induced pluripotent stem cell model (iPSC) of anthracycline-induced cardiotoxicity (ACT) from patients with ... ...

Abstract	Cancer therapies with anthracyclines have been shown to induce cardiovascular complications. The aims of this study were to establish an in vitro induced pluripotent stem cell model (iPSC) of anthracycline-induced cardiotoxicity (ACT) from patients with an aggressive form of B-cell lymphoma and to examine whether doxorubicin (DOX)-treated ACT-iPSC cardiomyocytes (CM) can recapitulate the clinical features exhibited by patients, and thus help uncover a DOX-dependent pathomechanism. ACT-iPSC CM generated from individuals with CD20
MeSH term(s)	Cardiotoxicity/metabolism ; Cardiotoxicity/pathology ; Doxorubicin/metabolism ; Doxorubicin/toxicity ; Heart Diseases/metabolism ; Heart Failure/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Myocytes, Cardiac/metabolism ; Neoplasms/metabolism
Chemical Substances	Doxorubicin (80168379AG)
Language	English
Publishing date	2022-03-08
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-022-00918-7
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Article ; Online: Redox regulation of cardiac hypertrophy.

Sag, Can M / Santos, Celio X C / Shah, Ajay M

Journal of molecular and cellular cardiology

2014 Volume 73, Page(s) 103–111

Abstract: It is increasingly evident that redox-dependent modifications in cellular proteins and signaling pathways (or redox signaling) play important roles in many aspects of cardiac hypertrophy. Indeed, these redox modifications may be intricately linked with ... ...

Abstract	It is increasingly evident that redox-dependent modifications in cellular proteins and signaling pathways (or redox signaling) play important roles in many aspects of cardiac hypertrophy. Indeed, these redox modifications may be intricately linked with the process of hypertrophy wherein there is not only a significant increase in myocardial O2 consumption but also important alterations in metabolic processes and in the local generation of O2-derived reactive species (ROS) that modulate and/or amplify cell signaling pathways. This article reviews our current knowledge of redox signaling pathways and their roles in cardiac hypertrophy. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".
MeSH term(s)	Animals ; Cardiomegaly/metabolism ; Humans ; NADPH Oxidases/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Signal Transduction/physiology
Chemical Substances	Reactive Oxygen Species ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2014-02-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2014.02.002
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