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  1. Article: Editorial: HFpEF and HFmrEF: Different Sides of the Same Coin?

    Martínez-Sellés, Manuel / Xu, Dachun / Zhang, Jian / Ong, Sang-Bing

    Frontiers in cardiovascular medicine

    2022  Volume 9, Page(s) 916534

    Language English
    Publishing date 2022-05-05
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2022.916534
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  2. Article: Editorial: Organellar dynamics in cell fate.

    Li, Yuzhen / Yao, Xianglan / Levine, Stewart J / Ong, Sang-Bing

    Frontiers in molecular biosciences

    2022  Volume 9, Page(s) 977014

    Language English
    Publishing date 2022-08-05
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2022.977014
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  3. Article: Large animal models of cardiac ischemia-reperfusion injury: Where are we now?

    Rahman, Attaur / Li, Yuhao / Chan, To-Kiu / Zhao, Hui / Xiang, Yaozu / Chang, Xing / Zhou, Hao / Xu, Dachun / Ong, Sang-Bing

    Zoological research

    2023  Volume 44, Issue 3, Page(s) 591–603

    Abstract: Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical ... ...

    Abstract Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical cardiovascular research are often limited to small animal models, which are not transferable or reproducible in large animal models due to different factors such as: (i) complex and varied features of human ischemic cardiac disease (ICD), which are challenging to mimic in animal models, (ii) significant differences in surgical techniques applied, and (iii) differences in cardiovascular anatomy and physiology between small versus large animals. This article highlights the advantages and disadvantages of different large animal models of preclinical cardiac ischemic reperfusion injury (IRI), as well as the different methods used to induce and assess IRI, and the obstacles faced in using large animals for translational research in the settings of cardiac IR.
    MeSH term(s) Humans ; Animals ; Myocardial Reperfusion Injury/veterinary ; Disease Models, Animal
    Language English
    Publishing date 2023-05-06
    Publishing country China
    Document type Journal Article ; Review
    ISSN 2095-8137
    ISSN 2095-8137
    DOI 10.24272/j.issn.2095-8137.2022.487
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  4. Article ; Online: Harnessing mitochondrial transplantation to sustain cardiac function: Another step forward.

    Li, Yuhao / Chinda, Kroekkiat / Xiang, Yaozu / Zhou, Hao / Xu, Dachun / Ong, Sang-Ging / Ong, Sang-Bing

    Molecular therapy : the journal of the American Society of Gene Therapy

    2023  Volume 31, Issue 5, Page(s) 1201–1203

    MeSH term(s) Mitochondria/genetics ; Myocardium/metabolism
    Language English
    Publishing date 2023-05-03
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2010592-7
    ISSN 1525-0024 ; 1525-0016
    ISSN (online) 1525-0024
    ISSN 1525-0016
    DOI 10.1016/j.ymthe.2023.04.003
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5640: Show issues Location:
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  5. Article ; Online: PEDF inhibits VEGF-induced vascular leakage through binding to VEGFR2 in acute myocardial infarction.

    Hui, Hong-Liang / Jiang, Bo / Zhou, Yan-Ying / Qiu, Fan / Lin, Yan-Gui / Li, Hua-Ming / Li, Dan / Luo, Min / Miao, Hao-Ran / Ong, Sang-Bing / Zhang, Yi-Qian

    Journal of biomolecular structure & dynamics

    2024  , Page(s) 1–13

    Abstract: Pigment epithelium-derived factor (PEDF) could bind to vascular endothelial growth factor receptor 2 (VEGFR2) and inhibit its activation induced by VEGF. But how PEDF affects VEGFR2 pathway is still poorly understood. In this study, we elucidated the ... ...

    Abstract Pigment epithelium-derived factor (PEDF) could bind to vascular endothelial growth factor receptor 2 (VEGFR2) and inhibit its activation induced by VEGF. But how PEDF affects VEGFR2 pathway is still poorly understood. In this study, we elucidated the precise mechanism underlying the interaction between PEDF and VEGFR2, and subsequently corroborated our findings using a rat AMI model. PEDF prevented endocytosis of VE-cadherin induced by hypoxia, thereby protecting the endothelium integrity. A three-dimensional model of the VEGFR2-PEDF complex was constructed by protein-protein docking method. The results showed that the VEGFR2-PEDF complex was stable during the simulation. Hydrogen bonds, binding energy and binding modes were analyzed during molecular dynamics simulations, which indicated that hydrogen bonds and hydrophobic interactions were important for the recognition of VEGFR2 with PEDF. In addition, the results from exudation of fibrinogen suggested that PEDF inhibits vascular leakage in acute myocardial infarction and confirmed the critical role of key amino acids in the regulation of endothelial cell permeability. This observation is also supported by echocardiography studies showing that the 34mer peptide sustained cardiac function during acute myocardial infarction. Besides, PEDF and 34mer could inhibit the aggregation of myofiber in the heart and promoted the formation of a dense cell layer in cardiomyocytes, which suggested that PEDF and 34mer peptide protect against AMI-induced cardiac dysfunction. These results suggest that PEDF inhibits the phosphorylation of downstream proteins, thereby preventing vascular leakage, which provides a new therapeutic direction for the treatment of acute myocardial infarction.Communicated by Ramaswamy H. Sarma.
    Language English
    Publishing date 2024-02-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 49157-3
    ISSN 1538-0254 ; 0739-1102
    ISSN (online) 1538-0254
    ISSN 0739-1102
    DOI 10.1080/07391102.2024.2314260
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    Zs.A 2093: Show issues Location:
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  6. Article ; Online: Integrated Stress Response Potentiates Ponatinib-Induced Cardiotoxicity.

    Yan, Gege / Han, Zhenbo / Kwon, Youjeong / Jousma, Jordan / Nukala, Sarath Babu / Prosser, Benjamin L / Du, Xiaoping / Pinho, Sandra / Ong, Sang-Bing / Lee, Won Hee / Ong, Sang-Ging

    Circulation research

    2024  Volume 134, Issue 5, Page(s) 482–501

    Abstract: Background: Mitochondrial dysfunction is a primary driver of cardiac contractile failure; yet, the cross talk between mitochondrial energetics and signaling regulation remains obscure. Ponatinib, a tyrosine kinase inhibitor used to treat chronic myeloid ...

    Abstract Background: Mitochondrial dysfunction is a primary driver of cardiac contractile failure; yet, the cross talk between mitochondrial energetics and signaling regulation remains obscure. Ponatinib, a tyrosine kinase inhibitor used to treat chronic myeloid leukemia, is among the most cardiotoxic tyrosine kinase inhibitors and causes mitochondrial dysfunction. Whether ponatinib-induced mitochondrial dysfunction triggers the integrated stress response (ISR) to induce ponatinib-induced cardiotoxicity remains to be determined.
    Methods: Using human induced pluripotent stem cells-derived cardiomyocytes and a recently developed mouse model of ponatinib-induced cardiotoxicity, we performed proteomic analysis, molecular and biochemical assays to investigate the relationship between ponatinib-induced mitochondrial stress and ISR and their role in promoting ponatinib-induced cardiotoxicity.
    Results: Proteomic analysis revealed that ponatinib activated the ISR in cardiac cells. We identified GCN2 (general control nonderepressible 2) as the eIF2α (eukaryotic translation initiation factor 2α) kinase responsible for relaying mitochondrial stress signals to trigger the primary ISR effector-ATF4 (activating transcription factor 4), upon ponatinib exposure. Mechanistically, ponatinib treatment exerted inhibitory effects on ATP synthase activity and reduced its expression levels resulting in ATP deficits. Perturbed mitochondrial function resulting in ATP deficits then acts as a trigger of GCN2-mediated ISR activation, effects that were negated by nicotinamide mononucleotide, an NAD
    Conclusions: Neutralizing ISR hyperactivation could prevent or reverse ponatinib-induced cardiotoxicity. The findings that compromised ATP production potentiates GCN2-mediated ISR activation have broad implications across various cardiac diseases. Our results also highlight an unanticipated role of ponatinib in causing direct activation of a kinase target despite its role as an ATP-competitive kinase inhibitor.
    MeSH term(s) Humans ; Animals ; Mice ; Protein Serine-Threonine Kinases/metabolism ; Cardiotoxicity/pathology ; Proteomics ; Induced Pluripotent Stem Cells/metabolism ; Myocytes, Cardiac/metabolism ; Protein Kinase Inhibitors/toxicity ; Mitochondrial Diseases/pathology ; Adenosine Triphosphate ; Imidazoles ; Pyridazines
    Chemical Substances Protein Serine-Threonine Kinases (EC 2.7.11.1) ; ponatinib (4340891KFS) ; Protein Kinase Inhibitors ; Adenosine Triphosphate (8L70Q75FXE) ; Imidazoles ; Pyridazines
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323683
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    Ui IV Zs.70: Show issues Location:
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  7. Article ; Online: Downregulation of Mitochondrial Fusion Protein Expression Affords Protection from Canonical Necroptosis in H9c2 Cardiomyoblasts.

    Toda, Yuki / Ong, Sang-Bing / Yano, Toshiyuki / Kuno, Atsushi / Kouzu, Hidemichi / Sato, Tatsuya / Ohwada, Wataru / Tatekoshi, Yuki / Ogawa, Toshifumi / Shimizu, Masaki / Tanno, Masaya / Furuhashi, Masato

    International journal of molecular sciences

    2024  Volume 25, Issue 5

    Abstract: Necroptosis, a form of necrosis, and alterations in mitochondrial dynamics, a coordinated process of mitochondrial fission and fusion, have been implicated in the pathogenesis of cardiovascular diseases. This study aimed to determine the role of ... ...

    Abstract Necroptosis, a form of necrosis, and alterations in mitochondrial dynamics, a coordinated process of mitochondrial fission and fusion, have been implicated in the pathogenesis of cardiovascular diseases. This study aimed to determine the role of mitochondrial morphology in canonical necroptosis induced by a combination of TNFα and zVAD (TNF/zVAD) in H9c2 cells, rat cardiomyoblasts. Time-course analyses of mitochondrial morphology showed that mitochondria were initially shortened after the addition of TNF/zVAD and then their length was restored, and the proportion of cells with elongated mitochondria at 12 h was larger in TNF/zVAD-treated cells than in non-treated cells (16.3 ± 0.9% vs. 8.0 ± 1.2%). The knockdown of dynamin-related protein 1 (Drp1) and fission 1, fission promoters, and treatment with Mdivi-1, a Drp-1 inhibitor, had no effect on TNF/zVAD-induced necroptosis. In contrast, TNF/zVAD-induced necroptosis was attenuated by the knockdown of mitofusin 1/2 (Mfn1/2) and optic atrophy-1 (Opa1), proteins that are indispensable for mitochondrial fusion, and the attenuation of necroptosis was not canceled by treatment with Mdivi-1. The expression of TGFβ-activated kinase (TAK1), a negative regulator of RIP1 activity, was upregulated and the TNF/zVAD-induced RIP1-Ser166 phosphorylation, an index of RIP1 activity, was mitigated by the knockdown of Mfn1/2 or Opa1. Pharmacological TAK1 inhibition attenuated the protection afforded by Mfn1/2 and Opa1 knockdown. In conclusion, the inhibition of mitochondrial fusion increases TAK1 expression, leading to the attenuation of canonical necroptosis through the suppression of RIP1 activity.
    MeSH term(s) Rats ; Animals ; Down-Regulation ; Necroptosis ; Mitochondrial Dynamics ; Necrosis/metabolism ; Mitochondria/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2024-03-02
    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/ijms25052905
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  8. Article: Mitochondrial Dynamics as a Therapeutic Target for Treating Cardiac Diseases.

    Ong, Sang-Bing / Hausenloy, Derek J

    Handbook of experimental pharmacology

    2016  Volume 240, Page(s) 251–279

    Abstract: Mitochondria are dynamic in nature and are able to shift their morphology between elongated interconnected mitochondrial networks and a fragmented disconnected arrangement by the processes of mitochondrial fusion and fission, respectively. Changes in ... ...

    Abstract Mitochondria are dynamic in nature and are able to shift their morphology between elongated interconnected mitochondrial networks and a fragmented disconnected arrangement by the processes of mitochondrial fusion and fission, respectively. Changes in mitochondrial morphology are regulated by the mitochondrial fusion proteins - mitofusins 1 and 2 (Mfn1 and 2), and optic atrophy 1 (Opa1) as well as the mitochondrial fission proteins - dynamin-related peptide 1 (Drp1) and fission protein 1 (Fis1). Despite having a unique spatial arrangement, cardiac mitochondria have been implicated in a variety of disorders including ischemia-reperfusion injury (IRI), heart failure, diabetes, and pulmonary hypertension. In this chapter, we review the influence of mitochondrial dynamics in these cardiac disorders as well as their potential as therapeutic targets in tackling cardiovascular disease.
    MeSH term(s) Animals ; Apoptosis ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/physiopathology ; Heart Diseases/drug therapy ; Heart Diseases/physiopathology ; Heart Failure/drug therapy ; Heart Failure/physiopathology ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/physiopathology ; Mitochondria, Heart/physiology ; Mitochondrial Dynamics/drug effects ; Mitochondrial Dynamics/physiology ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/physiopathology
    Language English
    Publishing date 2016-11-14
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 0171-2004
    ISSN 0171-2004
    DOI 10.1007/164_2016_7
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    Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
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  9. Article: The Calcineurin-Drp1-Mediated Mitochondrial Fragmentation Is Aligned with the Differentiation of c-Kit Cardiac Progenitor Cells.

    Rahman, Attaur / Li, Yuhao / Ismail, Nur Izzah / Chan, To-Kiu / Li, Yuzhen / Xu, Dachun / Zhou, Hao / Ong, Sang-Bing

    International journal of stem cells

    2022  Volume 16, Issue 2, Page(s) 123–134

    Abstract: Objective: The heart contains a pool of c-kit: Methods and results: c-kit: Conclusions: The findings from this study provide an alternative view of the role of mitochondrial fusion-fission in the differentiation of cardiac progenitor cells and the ...

    Abstract Objective: The heart contains a pool of c-kit
    Methods and results: c-kit
    Conclusions: The findings from this study provide an alternative view of the role of mitochondrial fusion-fission in the differentiation of cardiac progenitor cells and the potential of pharmacologically manipulating the mitochondria to direct progenitor cell fate.
    Language English
    Publishing date 2022-12-31
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2914134-5
    ISSN 2005-5447 ; 2005-3606
    ISSN (online) 2005-5447
    ISSN 2005-3606
    DOI 10.15283/ijsc22141
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  10. Article ; Online: Long COVID-19 and the Heart: Is Cardiac Mitochondria the Missing Link?

    Chang, Xing / Ismail, Nur Izzah / Rahman, Attaur / Xu, Dachun / Chan, Renee Wan Yi / Ong, Sang-Ging / Ong, Sang-Bing

    Antioxidants & redox signaling

    2022  Volume 38, Issue 7-9, Page(s) 599–618

    Abstract: Significance: ...

    Abstract Significance:
    MeSH term(s) Humans ; COVID-19/complications ; Post-Acute COVID-19 Syndrome ; SARS-CoV-2 ; Cardiovascular Diseases/etiology ; Heart Diseases ; Myocarditis/complications ; Myocarditis/therapy ; Mitochondria
    Language English
    Publishing date 2022-12-28
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2022.0126
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