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Article: Cardiac Autophagy in Sepsis.

Sun, Yuxiao / Cai, Ying / Zang, Qun S

2019 Volume 8, Issue 2

Abstract: Sepsis is a leading cause of death in intensive care units, and cardiac dysfunction is an identified serious component of the multi-organ failure associated with this critical condition. This review summarized the current discoveries and hypothesizes of ... ...

Abstract	Sepsis is a leading cause of death in intensive care units, and cardiac dysfunction is an identified serious component of the multi-organ failure associated with this critical condition. This review summarized the current discoveries and hypothesizes of how autophagy changes in the heart during sepsis and the underlying mechanisms. Recent investigations suggest that specific activation of autophagy initiation factor Beclin-1 has a potential to protect cardiac mitochondria, attenuate inflammation, and improve cardiac function in sepsis. Accordingly, pharmacological interventions targeting this pathway have a potential to become an effective approach to control sepsis outcomes. The role of autophagy during sepsis pathogenesis has been under intensive investigation in recent years. It is expected that developing therapeutic approaches with specificities targeting at autophagy regulatory factors may provide new opportunities to alleviate organ dysfunction caused by maladaptive autophagy during sepsis.
MeSH term(s)	Animals ; Autophagy ; Beclin-1/metabolism ; Humans ; Mitochondria, Heart/metabolism ; Mitophagy ; Myocardium/pathology ; Sepsis/pathology ; Sepsis/therapy
Chemical Substances	Beclin-1
Language	English
Publishing date	2019-02-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8020141
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Article ; Online: Beclin-1-Dependent Autophagy Improves Outcomes of Pneumonia-Induced Sepsis.

Nikouee, Azadeh / Kim, Matthew / Ding, Xiangzhong / Sun, Yuxiao / Zang, Qun S

Frontiers in cellular and infection microbiology

2021 Volume 11, Page(s) 706637

Abstract: Objective: We previously demonstrated that promoting Beclin-1-dependent autophagy is cardiac protective during endotoxemia shock, suggesting that autophagy-based approaches may become a promising therapeutic strategy for sepsis. In this study, we ... ...

Abstract	Objective: We previously demonstrated that promoting Beclin-1-dependent autophagy is cardiac protective during endotoxemia shock, suggesting that autophagy-based approaches may become a promising therapeutic strategy for sepsis. In this study, we applied both genetic and pharmacological approaches to evaluate whether Beclin-1 activation improves sepsis outcomes in a model of pneumonia-induced sepsis. Methods: Sepsis was induced in mice by Results: Pulmonary infection by Conclusion: Data suggest that targeted activation of Beclin-1 alleviates adverse outcomes of pneumonia-induced sepsis, and thus, possess a therapeutic potential.
MeSH term(s)	Animals ; Autophagy ; Beclin-1 ; Mice ; Mice, Inbred C57BL ; Pneumonia ; Sepsis/complications
Chemical Substances	Beclin-1
Language	English
Publishing date	2021-06-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2021.706637
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Article ; Online: Beclin-1 improves mitochondria-associated membranes in the heart during endotoxemia.

Sun, Yuxiao / Cai, Ying / Qian, Suhong / Chiou, Hellen / Zang, Qun S

FASEB bioAdvances

2021 Volume 3, Issue 3, Page(s) 123–135

Abstract: Mitochondria-associated membranes (MAMs) are essential to mitochondria. This study was to determine whether endotoxemia rearranges MAMs in the heart, and whether Beclin-1 regulates this process. Wild-type mice and mice with a cardiac-specific ... ...

Abstract	Mitochondria-associated membranes (MAMs) are essential to mitochondria. This study was to determine whether endotoxemia rearranges MAMs in the heart, and whether Beclin-1 regulates this process. Wild-type mice and mice with a cardiac-specific overexpression of Beclin-1 (
Language	English
Publishing date	2021-01-25
Publishing country	United States
Document type	Journal Article
ISSN	2573-9832
ISSN (online)	2573-9832
DOI	10.1096/fba.2020-00039
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Article: Metabolic and inflammatory functions of cannabinoid receptor type 1 are differentially modulated by adiponectin.

Wei, Qiong / Lee, Jong Han / Wu, Chia-Shan / Zang, Qun S / Guo, Shaodong / Lu, Hui-Chen / Sun, Yuxiang

World journal of diabetes

2021 Volume 12, Issue 10, Page(s) 1750–1764

Abstract: Background: Antagonists of cannabinoid type 1 receptor (: Aim: To investigate whether the beneficial effects of : Methods: We compared metabolic and inflammatory phenotypes of wild-type (WT) mice, : Results: CB1: Conclusion: Our findings ... ...

Abstract	Background: Antagonists of cannabinoid type 1 receptor ( Aim: To investigate whether the beneficial effects of Methods: We compared metabolic and inflammatory phenotypes of wild-type (WT) mice, Results: CB1 Conclusion: Our findings reveal that
Language	English
Publishing date	2021-11-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2583471-X
ISSN	1948-9358
ISSN	1948-9358
DOI	10.4239/wjd.v12.i10.1750
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Article: Sepsis-induced Cardiac Mitochondrial Damage and Potential Therapeutic Interventions in the Elderly.

Zang, Qun S / Wolf, Steven E / Minei, Joseph P

Aging and disease

2014 Volume 5, Issue 2, Page(s) 137–149

Abstract: The incidence of sepsis and its attendant mortality risk are significantly increased with aging. Thus, severe sepsis in the elderly is likely to become an emerging concern in critical care units. Cardiac dysfunction is an important component of multi- ... ...

Abstract	The incidence of sepsis and its attendant mortality risk are significantly increased with aging. Thus, severe sepsis in the elderly is likely to become an emerging concern in critical care units. Cardiac dysfunction is an important component of multi-organ failure after sepsis. In our laboratory, utilizing a pneumonia-related sepsis animal model, our research has been focused on the mechanisms underlying sepsis-induced cardiac failure. In this review, based on findings from others and ours, we discussed age-dependent decay in mitochondria and the role of mitochondrial reactive oxygen species (mtROS) in sepsis-induced cardiac inflammation and autophagy. Our recent discovery of a potential signal transduction pathway that triggers myocardial mitochondrial damage is also discussed. Because of the significance of mitochondria damage in the aging process and in sepsis pathogenesis, we hypothesize that specific enhancing mitochondrial antioxidant defense by mitochondria-targeted antioxidants (MTAs) may provide important therapeutic potential in treating elder sepsis patients. In this review, we summarized the categories of currently published MTA molecules and the results of preclinical evaluation of MTAs in sepsis and aging models.
Language	English
Publishing date	2014-04-01
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2014.0500137
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Article ; Online: Burn Serum Stimulates Myoblast Cell Death Associated with IL-6-Induced Mitochondrial Fragmentation.

Sehat, Alvand / Huebinger, Ryan M / Carlson, Deborah L / Zang, Qun S / Wolf, Steven E / Song, Juquan

Shock (Augusta, Ga.)

2017 Volume 48, Issue 2, Page(s) 236–242

Abstract: Background: Burn patients suffer muscle mass loss associated with hyperinflammation and hypercatabolism. The mitochondria are affected by this metabolic alteration. Mitochondrial fission activates a caspase cascade that ultimately leads to cell death. ... ...

Abstract	Background: Burn patients suffer muscle mass loss associated with hyperinflammation and hypercatabolism. The mitochondria are affected by this metabolic alteration. Mitochondrial fission activates a caspase cascade that ultimately leads to cell death. We postulate that burn-induced muscle loss is associated with increased mitochondrial fission and subsequent functional impairment. Further, we investigated whether the cytokine IL-6 plays a major role in mitochondrial fission-associated cell death after burn. Methods: Murine myoblast C2C12 cells were treated with 10% serum isolated either from control rats or 40% total body surface area burned rats. Mitochondria were labeled with MitoTracker Green for live cell images. Mitochondrial function was assessed with an Enzo Mito-ID membrane potential cytotoxicity kit. Protein signals were detected by Western blot analysis. Moreover, recombinant IL-6 was applied to stimulate C2C12 to differentiate the role of cytokine IL-6; lastly, we treated burn serum-stimulated cells with IL-6 antibodies. Results: Caspase 3 activity increased in C2C12 cells with burn serum stimulation, suggesting increased cell death in skeletal muscle after burn. Mitochondrial morphology shortened and mitochondrial membrane potential decreased in cells treated with burn serum. Western blot data showed that mitofusion-1 expression significantly decreased in burn serum-treated cells, supporting the morphologic observation of mitochondrial fission. Mitochondrial fragmentation increased with IL-6 stimulation, and IL-6 antibody decreased caspase 3 activity and mitochondrial membrane potential improved in burn serum-stimulated cells. Conclusion: Burn serum caused muscle cell death associated with increased mitochondrial fission and functional impairment. This alteration was alleviated with IL-6 antibody treatment, suggesting the cytokine plays a role in mitochondrial changes in muscle after systemic injury.
MeSH term(s)	Animals ; Burns/blood ; Cell Death ; Cell Line ; Interleukin-6/metabolism ; Mice ; Mitochondria, Muscle/metabolism ; Mitochondria, Muscle/pathology ; Myoblasts, Skeletal/metabolism ; Myoblasts, Skeletal/pathology ; Serum
Chemical Substances	Interleukin-6 ; interleukin-6, mouse
Language	English
Publishing date	2017-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000000846
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Article ; Online: aP2-Cre Mediated Ablation of GHS-R Attenuates Adiposity and Improves Insulin Sensitivity during Aging.

Lin, Ligen / Lee, Jong Han / Wang, Ruitao / Wang, Ru / Sheikh-Hamad, David / Zang, Qun S / Sun, Yuxiang

International journal of molecular sciences

2018 Volume 19, Issue 10

Abstract: Ghrelin via its receptor, the growth hormone secretagogue receptor (GHS-R), increases food intake and adiposity. The tissue-specific functions of GHS-R in peripheral tissues are mostly unknown. We previously reported that while GHS-R expression is very ... ...

Abstract	Ghrelin via its receptor, the growth hormone secretagogue receptor (GHS-R), increases food intake and adiposity. The tissue-specific functions of GHS-R in peripheral tissues are mostly unknown. We previously reported that while GHS-R expression is very low in white and brown fat of young mice, expression increases during aging. To investigate whether GHS-R has cell-autonomous effects in adipose tissues, we generated
MeSH term(s)	Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Adiposity/drug effects ; Aging/metabolism ; Animals ; Carbohydrates/chemistry ; Eating/drug effects ; Energy Metabolism ; Fatty Acid-Binding Proteins/genetics ; Gene Deletion ; Gene Knockdown Techniques ; Ghrelin/pharmacology ; Glucose Tolerance Test ; Growth Hormone/metabolism ; Insulin Resistance ; Integrases/metabolism ; Lipolysis/drug effects ; Metabolomics ; Mice, Inbred C57BL ; Mice, Transgenic ; Proteins/metabolism ; Receptors, Ghrelin/metabolism ; Thermogenesis/drug effects
Chemical Substances	Carbohydrates ; Fabp4 protein, mouse ; Fatty Acid-Binding Proteins ; Ghrelin ; Proteins ; Receptors, Ghrelin ; Growth Hormone (9002-72-6) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2018-10-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19103002
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Article ; Online: Matricellular Protein Cilp1 Promotes Myocardial Fibrosis in Response to Myocardial Infarction.

Zhang, Qing-Jun / He, Yu / Li, Yongnan / Shen, Huali / Lin, Ling / Zhu, Min / Wang, Zhaoning / Luo, Xiang / Hill, Joseph A / Cao, Dian / Luo, Richard L / Zou, Raymond / McAnally, John / Liao, Jun / Bajona, Pietro / Zang, Qun S / Yu, Yonghao / Liu, Zhi-Ping

Circulation research

2021 Volume 129, Issue 11, Page(s) 1021–1035

Abstract: Figure: see text]. ...

Abstract	[Figure: see text].
MeSH term(s)	Animals ; Cells, Cultured ; Fibrosis ; HEK293 Cells ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Pyrophosphatases/genetics ; Pyrophosphatases/metabolism
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; CILP protein, mouse (EC 3.6.1.-) ; Pyrophosphatases (EC 3.6.1.-)
Language	English
Publishing date	2021-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.319482
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Article ; Online: Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model.

Yao, Xiao / Carlson, Deborah / Sun, Yuxiao / Ma, Lisha / Wolf, Steven E / Minei, Joseph P / Zang, Qun S

PloS one

2015 Volume 10, Issue 10, Page(s) e0139416

Abstract: We have previously shown that mitochondria-targeted vitamin E (Mito-Vit-E), a mtROS specific antioxidant, improves cardiac performance and attenuates inflammation in a pneumonia-related sepsis model. In this study, we applied the same approaches to ... ...

Abstract	We have previously shown that mitochondria-targeted vitamin E (Mito-Vit-E), a mtROS specific antioxidant, improves cardiac performance and attenuates inflammation in a pneumonia-related sepsis model. In this study, we applied the same approaches to decipher the signaling pathway(s) of mtROS-dependent cardiac inflammation after sepsis. Sepsis was induced in Sprague Dawley rats by intratracheal injection of S. pneumoniae. Mito-Vit-E, vitamin E or vehicle was administered 30 minutes later. In myocardium 24 hours post-inoculation, Mito-Vit-E, but not vitamin E, significantly protected mtDNA integrity and decreased mtDNA damage. Mito-Vit-E alleviated sepsis-induced reduction in mitochondria-localized DNA repair enzymes including DNA polymerase γ, AP endonuclease, 8-oxoguanine glycosylase, and uracil-DNA glycosylase. Mito-Vit-E dramatically improved metabolism and membrane integrity in mitochondria, suppressed leakage of mtDNA into the cytoplasm, inhibited up-regulation of Toll-like receptor 9 (TLR9) pathway factors MYD88 and RAGE, and limited RAGE interaction with its ligand TFAM in septic hearts. Mito-Vit-E also deactivated NF-κB and caspase 1, reduced expression of the essential inflammasome component ASC, and decreased inflammatory cytokine IL-1β. In vitro, both Mito-Vit-E and TLR9 inhibitor OND-I suppressed LPS-induced up-regulation in MYD88, RAGE, ASC, active caspase 1, and IL-1β in cardiomyocytes. Since free mtDNA escaped from damaged mitochondria function as a type of DAMPs to stimulate inflammation through TLR9, these data together suggest that sepsis-induced cardiac inflammation is mediated, at least partially, through mtDNA-TLR9-RAGE. At last, Mito-Vit-E reduced the circulation of myocardial injury marker troponin-I, diminished apoptosis and amended morphology in septic hearts, suggesting that mitochondria-targeted antioxidants are a potential cardioprotective approach for sepsis.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Cells, Cultured ; DNA, Mitochondrial/metabolism ; Disease Models, Animal ; Interleukin-1beta/analysis ; Lipopolysaccharides/toxicity ; Male ; Mitochondria/drug effects ; Mitochondria/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Reactive Oxygen Species/toxicity ; Sepsis/etiology ; Sepsis/metabolism ; Signal Transduction/drug effects ; Streptococcus pneumoniae/pathogenicity ; Superoxides/metabolism ; Superoxides/toxicity ; Toll-Like Receptor 9/antagonists & inhibitors ; Toll-Like Receptor 9/metabolism ; Troponin/analysis ; Vitamin E/pharmacology
Chemical Substances	Antioxidants ; DNA, Mitochondrial ; Interleukin-1beta ; Lipopolysaccharides ; Reactive Oxygen Species ; Toll-Like Receptor 9 ; Troponin ; Superoxides (11062-77-4) ; Vitamin E (1406-18-4)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0139416
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Article ; Online: Deficiency in Heat Shock Factor 1 (HSF-1) Expression Exacerbates Sepsis-induced Inflammation and Cardiac Dysfunction.

Barber, Robert C / Maass, David L / White, D Jean / Horton, Jureta W / Wolf, Steven E / Minei, Joseph P / Zang, Qun S

SOJ surgery

2014 Volume 1, Issue 1

Abstract: In the present study, we investigated whether absence of heat shock factor 1 (HSF-1) and inability to increase myocardial expression of heat shock proteins alter septic responses of inflammatory cytokines and myocardial contractility. HSF-1 knockout ( ...

Abstract	In the present study, we investigated whether absence of heat shock factor 1 (HSF-1) and inability to increase myocardial expression of heat shock proteins alter septic responses of inflammatory cytokines and myocardial contractility. HSF-1 knockout (
Language	English
Publishing date	2014-01-27
Publishing country	United States
Document type	Journal Article
ISSN	2376-4570
ISSN (online)	2376-4570
DOI	10.15226/2376-4570/1/1/00103
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