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Article ; Online: The Role of Alternative Mitophagy in Heart Disease.

Nah, Jihoon

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: Autophagy is essential for maintaining cellular homeostasis through bulk degradation of subcellular constituents, including misfolded proteins and dysfunctional organelles. It is generally governed by the proteins Atg5 and Atg7, which are critical ... ...

Abstract	Autophagy is essential for maintaining cellular homeostasis through bulk degradation of subcellular constituents, including misfolded proteins and dysfunctional organelles. It is generally governed by the proteins Atg5 and Atg7, which are critical regulators of the conventional autophagy pathway. However, recent studies have identified an alternative Atg5/Atg7-independent pathway, i.e., Ulk1- and Rab9-mediated alternative autophagy. More intensive studies have identified its essential role in stress-induced mitochondrial autophagy, also known as mitophagy. Alternative mitophagy plays pathophysiological roles in heart diseases such as myocardial ischemia and pressure overload. Here, this review discusses the established and emerging mechanisms of alternative autophagy/mitophagy that can be applied in therapeutic interventions for heart disorders.
MeSH term(s)	Humans ; Mitophagy ; Autophagy/physiology ; Myocardial Ischemia/metabolism ; Mitochondria/metabolism
Language	English
Publishing date	2023-03-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076362
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Article ; Online: The role of autophagic cell death in cardiac disease.

Nah, Jihoon / Zablocki, Daniela / Sadoshima, Junichi

Journal of molecular and cellular cardiology

2022 Volume 173, Page(s) 16–24

Abstract: Cardiomyocytes undergo various forms of cell death during heart disease such as myocardial infarction and heart failure. Understanding the mechanisms of cell death in cardiomyocytes is one of the most fundamental issues in the treatment of heart failure. ...

Abstract	Cardiomyocytes undergo various forms of cell death during heart disease such as myocardial infarction and heart failure. Understanding the mechanisms of cell death in cardiomyocytes is one of the most fundamental issues in the treatment of heart failure. Among the several kinds of cell death mechanisms, this review will focus on autophagy-related cardiomyocyte cell death. Although autophagy plays an essential role in mediating cellular quality control mechanisms for cell survival, dysregulation of autophagy can cause cell death, referred to as autophagy-dependent cell death or type II programmed cell death. The recent discovery of autosis as a modality of autophagy-dependent cell death with unique morphological and biochemical features has allowed us to broaden our understanding of the mechanistic role of autophagy in cell death. Here, we discuss autophagy-dependent cardiomyocyte cell death, including autosis, in pathophysiological conditions of the heart.
MeSH term(s)	Humans ; Autophagic Cell Death ; Autophagy/physiology ; Myocytes, Cardiac/metabolism ; Heart Diseases/metabolism ; Heart Failure/metabolism
Language	English
Publishing date	2022-09-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2022.08.362
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Zs.A 426: Show issues

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Article ; Online: The role of the Hippo pathway in autophagy in the heart.

Maejima, Yasuhiro / Zablocki, Daniela / Nah, Jihoon / Sadoshima, Junichi

Cardiovascular research

2022 Volume 118, Issue 17, Page(s) 3320–3330

Abstract: The Hippo pathway, an evolutionarily conserved signalling mechanism, controls organ size and tumourigenesis. Increasing lines of evidence suggest that autophagy, an important mechanism of lysosome-mediated cellular degradation, is regulated by the Hippo ... ...

Abstract	The Hippo pathway, an evolutionarily conserved signalling mechanism, controls organ size and tumourigenesis. Increasing lines of evidence suggest that autophagy, an important mechanism of lysosome-mediated cellular degradation, is regulated by the Hippo pathway, which thereby profoundly affects cell growth and death responses in various cell types. In the heart, Mst1, an upstream component of the Hippo pathway, not only induces apoptosis but also inhibits autophagy through phosphorylation of Beclin 1. YAP/TAZ, transcription factor co-factors and the terminal effectors of the Hippo pathway, affect autophagy through transcriptional activation of TFEB, a master regulator of autophagy and lysosomal biogenesis. The cellular abundance of YAP is negatively regulated by autophagy and suppression of autophagy induces accumulation of YAP, which, in turn, acts as a feedback mechanism to induce autophagosome formation. Thus, the Hippo pathway and autophagy regulate each other, thereby profoundly affecting cardiomyocyte survival and death. This review discusses the interaction between the Hippo pathway and autophagy and its functional significance during stress conditions in the heart and the cardiomyocytes therein.
MeSH term(s)	Hippo Signaling Pathway ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Cell Cycle Proteins/metabolism ; Transcription Factors/metabolism ; Myocytes, Cardiac/metabolism ; Autophagy
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Cell Cycle Proteins ; Transcription Factors
Language	English
Publishing date	2022-02-12
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvac014
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Zs.A 565: Show issues

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Article ; Online: The roles of the inhibitory autophagy regulator Rubicon in the heart: A new therapeutic target to prevent cardiac cell death.

Nah, Jihoon / Zablocki, Daniela / Sadoshima, Junichi

Experimental & molecular medicine

2021 Volume 53, Issue 4, Page(s) 528–536

Abstract: Autophagy contributes to the maintenance of cardiac homeostasis. The level of autophagy is dynamically altered in heart disease. Although autophagy is a promising therapeutic target, only a few selective autophagy activator candidates have been reported ... ...

Abstract	Autophagy contributes to the maintenance of cardiac homeostasis. The level of autophagy is dynamically altered in heart disease. Although autophagy is a promising therapeutic target, only a few selective autophagy activator candidates have been reported thus far. Rubicon is one of the few endogenous negative regulators of autophagy and a potential target for autophagy-inducing therapeutics. Rubicon was initially identified as a component of the Class III PI3K complex, and it has multiple functions, not only in canonical autophagy but also in endosomal trafficking and inflammatory responses. This review summarizes the molecular action of Rubicon in canonical and noncanonical autophagy. We discuss the roles of Rubicon in cardiac stress and the therapeutic potential of Rubicon in cardiac diseases through its modulation of autophagy.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/metabolism ; Biomarkers ; Cell Death ; Disease Management ; Disease Susceptibility ; Endocytosis ; Heart/physiology ; Homeostasis ; Humans ; Molecular Targeted Therapy ; Myocardium/metabolism ; Signal Transduction
Chemical Substances	Autophagy-Related Proteins ; Biomarkers ; RUBCN protein, human
Language	English
Publishing date	2021-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-021-00600-3
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Zs.A 4775: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Autosis: A New Target to Prevent Cell Death.

Nah, Jihoon / Zablocki, Daniela / Sadoshima, Junichi

JACC. Basic to translational science

2020 Volume 5, Issue 8, Page(s) 857–869

Abstract: Excessive autophagy induces a defined form of cell death called autosis, which is characterized by unique morphological features, including ballooning of perinuclear space and biochemical features, including sensitivity to cardiac glycosides. Autosis is ... ...

Abstract	Excessive autophagy induces a defined form of cell death called autosis, which is characterized by unique morphological features, including ballooning of perinuclear space and biochemical features, including sensitivity to cardiac glycosides. Autosis is observed during the late phase of reperfusion after a period of ischemia and contributes to myocardial injury. This review discusses unique features of autosis, the involvement of autosis in myocardial injury, and the molecular mechanism of autosis. Because autosis promotes myocardial injury under some conditions, a better understanding of autosis may lead to development of novel interventions to protect the heart against myocardial stress.
Language	English
Publishing date	2020-08-24
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2020.04.014
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Article ; Online: Tfeb-Mediated Transcriptional Regulation of Autophagy Induces Autosis during Ischemia/Reperfusion in the Heart.

Nah, Jihoon / Sung, Eun-Ah / Zhai, Peiyong / Zablocki, Daniela / Sadoshima, Junichi

Cells

2022 Volume 11, Issue 2

Abstract: Autosis is a unique form of cell death with characteristic morphological and biochemical features caused by dysregulated autophagy. Autosis is observed in the heart during the late phase of ischemia/reperfusion (I/R), when marked accumulation of ... ...

Abstract	Autosis is a unique form of cell death with characteristic morphological and biochemical features caused by dysregulated autophagy. Autosis is observed in the heart during the late phase of ischemia/reperfusion (I/R), when marked accumulation of autophagosomes is induced. We previously showed that the excessive accumulation of autophagosomes promotes autosis in cardiomyocytes. Although the inhibition of autophagic flux via the upregulation of Rubicon induces the accumulation of autophagosomes during I/R, it appears that additional mechanisms exacerbating autophagosome accumulation are required for the induction of autosis. Here, we show that Tfeb contributes to the induction of autosis during the late phase of I/R in the heart. During myocardial reperfusion, Tfeb is activated and translocated into the nucleus, which in turn upregulates genes involved in autophagy and lysosomal function. The overexpression of Tfeb enhanced cardiomyocyte death induced by a high dose of TAT-Beclin 1, an effect that was inhibited by the downregulation of Atg7. Conversely, the knockdown of Tfeb attenuated high-dose TAT-Beclin1-induced death in cardiomyocytes. Although the downregulation of Tfeb in the heart significantly decreased the number of autophagic vacuoles and inhibited autosis during I/R, the activation of Tfeb activity via 3,4-dimethoxychalcone, an activator of Tfeb, aggravated myocardial injury during I/R. These findings suggest that Tfeb promotes cardiomyocyte autosis during the late phase of reperfusion in the heart.
MeSH term(s)	Animals ; Animals, Newborn ; Autophagy/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Beclin-1/metabolism ; Chalcones ; Down-Regulation/genetics ; Gene Expression Regulation ; Gene Products, tat/metabolism ; Lysosomes/metabolism ; Mice, Inbred C57BL ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/pathology ; Myocytes, Cardiac/metabolism ; Transcription, Genetic ; Up-Regulation/genetics ; Vacuoles/metabolism ; Mice
Chemical Substances	3,4-dimethoxychalcone ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Beclin-1 ; Chalcones ; Gene Products, tat ; Tcfeb protein, mouse
Language	English
Publishing date	2022-01-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11020258
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Article ; Online: Differential dynamics of cullin deneddylation via COP9 signalosome subunit 5 interaction.

Kim, Yeong-Mu / Kim, Hye-Ji / Kim, Dong-Kyu / Jung, Dong-Hyun / Cho, Hyo Je / Kim, Sangjune / Nah, Jihoon / Jang, Sang-Min

Biochemical and biophysical research communications

2022 Volume 637, Page(s) 341–347

Abstract: Cullin-RING E3 ubiquitin ligases (CRLs) spatiotemporally regulate the proteasomal degradation of numerous cellular proteins involved in cell cycle control, DNA replication, and maintenance of genome stability. Activation of CRLs is controlled via ... ...

Abstract	Cullin-RING E3 ubiquitin ligases (CRLs) spatiotemporally regulate the proteasomal degradation of numerous cellular proteins involved in cell cycle control, DNA replication, and maintenance of genome stability. Activation of CRLs is controlled via neddylation by NEDD8-activating, -conjugating, and -attaching enzymes to the C-terminus of scaffold cullins (CULs), whereas the COP9 signalosome (CSN) inactivates CRLs via deneddylation. Here, we show that the deneddylation rate of each CUL is differentially modulated. Dose- or time-dependent treatment with pevonedistat, a small molecule inhibitor of NEDD8-activating enzyme (NAE), rapidly inhibits neddylation in most CULs, including CUL1, CUL3, CUL4A/B, and CUL5, whereas the deneddylation of CUL2 is slowly increased. We revealed that the different deneddylation speeds of each CUL depend on its binding strength with CSN5, the catalytic core of the CSN complex. Immunoprecipitation analysis revealed that CUL2 has a lower binding affinity for CSN5 than other CULs. Consistently, released cells treated with CSN5 inhibitor showed that CUL2 was slowly converted to the deneddylated form compared to the rapid deneddylation of other CULs. These findings provide mechanistic insights into the different dynamics of CULs in neddylation-deneddylation conversion.
MeSH term(s)	COP9 Signalosome Complex ; Cullin Proteins ; Proteolysis ; Ubiquitin ; Cell Nucleus
Chemical Substances	COP9 Signalosome Complex (EC 3.4.19.12) ; Cullin Proteins ; Ubiquitin
Language	English
Publishing date	2022-11-16
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.2022.11.045
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Zs.A 116: Show issues

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Article ; Online: Mitophagy as a Protective Mechanism against Myocardial Stress.

Nah, Jihoon / Miyamoto, Shigeki / Sadoshima, Junichi

Comprehensive Physiology

2017 Volume 7, Issue 4, Page(s) 1407–1424

Abstract: Mitochondria are dynamic organelles that can undergo fusion, fission, biogenesis, and autophagic elimination to maintain mitochondrial quality control. Since the heart is in constant need of high amounts of energy, mitochondria, as a central energy ... ...

Abstract	Mitochondria are dynamic organelles that can undergo fusion, fission, biogenesis, and autophagic elimination to maintain mitochondrial quality control. Since the heart is in constant need of high amounts of energy, mitochondria, as a central energy supply source, play a crucial role in maintaining optimal cardiac performance. Therefore, it is reasonable to assume that mitochondrial dysfunction is associated with the pathophysiology of heart diseases. In non-dividing, post-mitotic cells such as cardiomyocytes, elimination of dysfunctional organelles is essential to maintaining cellular function because non-dividing cells cannot dilute dysfunctional organelles through cell division. In this review, we discuss the recent findings regarding the physiological role of mitophagy in the heart and cardiomyocytes. Moreover, we discuss the functional role of mitophagy in the progression of cardiovascular diseases, including myocardial ischemic injury, diabetic cardiomyopathy, cardiac hypertrophy, and heart failure. © 2017 American Physiological Society. Compr Physiol 7:1407-1424, 2017.
Language	English
Publishing date	2017-09-12
Publishing country	United States
Document type	Journal Article
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c170005
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Article ; Online: YAP plays a crucial role in the development of cardiomyopathy in lysosomal storage diseases.

Ikeda, Shohei / Nah, Jihoon / Shirakabe, Akihiro / Zhai, Peiyong / Oka, Shin-Ichi / Sciarretta, Sebastiano / Guan, Kun-Liang / Shimokawa, Hiroaki / Sadoshima, Junichi

The Journal of clinical investigation

2021 Volume 131, Issue 5

Abstract: Lysosomal dysfunction caused by mutations in lysosomal genes results in lysosomal storage disorder (LSD), characterized by accumulation of damaged proteins and organelles in cells and functional abnormalities in major organs, including the heart, ... ...

Abstract	Lysosomal dysfunction caused by mutations in lysosomal genes results in lysosomal storage disorder (LSD), characterized by accumulation of damaged proteins and organelles in cells and functional abnormalities in major organs, including the heart, skeletal muscle, and liver. In LSD, autophagy is inhibited at the lysosomal degradation step and accumulation of autophagosomes is observed. Enlargement of the left ventricle (LV) and contractile dysfunction were observed in RagA/B cardiac-specific KO (cKO) mice, a mouse model of LSD in which lysosomal acidification is impaired irreversibly. YAP, a downstream effector of the Hippo pathway, was accumulated in RagA/B cKO mouse hearts. Inhibition of YAP ameliorated cardiac hypertrophy and contractile dysfunction and attenuated accumulation of autophagosomes without affecting lysosomal function, suggesting that YAP plays an important role in mediating cardiomyopathy in RagA/B cKO mice. Cardiomyopathy was also alleviated by downregulation of Atg7, an intervention to inhibit autophagy, whereas it was exacerbated by stimulation of autophagy. YAP physically interacted with transcription factor EB (TFEB), a master transcription factor that controls autophagic and lysosomal gene expression, thereby facilitating accumulation of autophagosomes without degradation. These results indicate that accumulation of YAP in the presence of LSD promotes cardiomyopathy by stimulating accumulation of autophagosomes through activation of TFEB.
Language	English
Publishing date	2021-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI143173
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Article ; Online: Selective induction of Rab9-dependent alternative mitophagy using a synthetic derivative of isoquinoline alleviates mitochondrial dysfunction and cognitive deficits in Alzheimer's disease models.

Um, Jee-Hyun / Shin, Dong Jin / Choi, Se Myeong / Nathan, Alen Benhur Pravin / Kim, Young Yeon / Lee, Da Ye / Jeong, Dae Jin / Kim, Dong Hyun / Kim, Kyung Hwa / Kim, Young Hye / Nah, Jihoon / Jeong, Jeong-Hee / Yoo, Eunhee / Shin, Hwa Kyoung / Park, Hwan Tae / Jo, Jihoon / Cho, Jong Hyun / Yun, Jeanho

Theranostics

2024 Volume 14, Issue 1, Page(s) 56–74

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Mice ; Animals ; Alzheimer Disease/metabolism ; Mitophagy ; Neuroblastoma ; Disease Models, Animal ; Isoquinolines/pharmacology ; Mitochondrial Diseases ; Cognition
Chemical Substances	Isoquinolines
Language	English
Publishing date	2024-01-01
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.88718
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