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  1. Article ; Online: Inhibition of the mPTP and Lipid Peroxidation Is Additively Protective Against I/R Injury.

    Mendoza, Arielys / Patel, Pooja / Robichaux, Dexter / Ramirez, Daniel / Karch, Jason

    Circulation research

    2024  

    Abstract: Background: During myocardial ischemia/reperfusion (I/R) injury, high levels of matrix Ca: Methods: Here, we use a combination of isolated mitochondrial assays and in vivo I/R surgery in mice. We challenged isolated liver and heart mitochondria with ... ...

    Abstract Background: During myocardial ischemia/reperfusion (I/R) injury, high levels of matrix Ca
    Methods: Here, we use a combination of isolated mitochondrial assays and in vivo I/R surgery in mice. We challenged isolated liver and heart mitochondria with Ca
    Results: In the absence of Ca
    Conclusions: In the present study, we have investigated the relationship between Ca
    Language English
    Publishing date 2024-04-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323882
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Simultaneous Acquisition of Mitochondrial Calcium Retention Capacity and Swelling to Measure Permeability Transition Sensitivity.

    Mendoza, Arielys M / Karch, Jason

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2497, Page(s) 129–140

    Abstract: The loss of mitochondrial cristae integrity and mitochondrial swelling are hallmarks of multiple forms of necrotic cell death. One of the most well-studied and relevant inducers of mitochondrial swelling is matrix calcium ( ... ...

    Abstract The loss of mitochondrial cristae integrity and mitochondrial swelling are hallmarks of multiple forms of necrotic cell death. One of the most well-studied and relevant inducers of mitochondrial swelling is matrix calcium (Ca
    MeSH term(s) Calcium/metabolism ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore ; Mitochondrial Swelling ; Permeability
    Chemical Substances Calcium (SY7Q814VUP) ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore
    Language English
    Publishing date 2022-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2309-1_9
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  3. Article ; Online: Keeping the beat against time: Mitochondrial fitness in the aging heart.

    Mendoza, Arielys / Karch, Jason

    Frontiers in aging

    2022  Volume 3, Page(s) 951417

    Abstract: The process of aging strongly correlates with maladaptive architectural, mechanical, and biochemical alterations that contribute to the decline in cardiac function. Consequently, aging is a major risk factor for the development of heart disease, the ... ...

    Abstract The process of aging strongly correlates with maladaptive architectural, mechanical, and biochemical alterations that contribute to the decline in cardiac function. Consequently, aging is a major risk factor for the development of heart disease, the leading cause of death in the developed world. In this review, we will summarize the classic and recently uncovered pathological changes within the aged heart with an emphasis on the mitochondria. Specifically, we describe the metabolic changes that occur in the aging heart as well as the loss of mitochondrial fitness and function and how these factors contribute to the decline in cardiomyocyte number. In addition, we highlight recent pharmacological, genetic, or behavioral therapeutic intervention advancements that may alleviate age-related cardiac decline.
    Language English
    Publishing date 2022-07-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 3076785-4
    ISSN 2673-6217 ; 2673-6217
    ISSN (online) 2673-6217
    ISSN 2673-6217
    DOI 10.3389/fragi.2022.951417
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  4. Article ; Online: Mitochondrial permeability transition pore-dependent necrosis.

    Robichaux, Dexter J / Harata, Mikako / Murphy, Elizabeth / Karch, Jason

    Journal of molecular and cellular cardiology

    2022  Volume 174, Page(s) 47–55

    Abstract: Mitochondrial permeability transition pore (mPTP)-dependent cell death is a form of necrotic cell death that is driven by mitochondrial dysfunction by the opening of the mPTP and is triggered by increases in matrix levels of ... ...

    Abstract Mitochondrial permeability transition pore (mPTP)-dependent cell death is a form of necrotic cell death that is driven by mitochondrial dysfunction by the opening of the mPTP and is triggered by increases in matrix levels of Ca
    MeSH term(s) Humans ; Mitochondrial Permeability Transition Pore/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Necrosis/metabolism ; Myocardial Reperfusion Injury/metabolism ; Cell Death ; Mitochondria, Heart/metabolism
    Chemical Substances Mitochondrial Permeability Transition Pore ; Mitochondrial Membrane Transport Proteins
    Language English
    Publishing date 2022-11-21
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2022.11.003
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  5. Article ; Online: The molecular mosaic of regulated cell death in the cardiovascular system.

    Martens, Matthew D / Karch, Jason / Gordon, Joseph W

    Biochimica et biophysica acta. Molecular basis of disease

    2021  Volume 1868, Issue 1, Page(s) 166297

    Abstract: Cell death is now understood to be a highly regulated process that contributes to normal development and tissue homeostasis, alongside its role in the etiology of various pathological conditions. Through detailed molecular analysis, we have come to know ... ...

    Abstract Cell death is now understood to be a highly regulated process that contributes to normal development and tissue homeostasis, alongside its role in the etiology of various pathological conditions. Through detailed molecular analysis, we have come to know that all cells do not always die in the same way, and that there are at least 7 processes involved, including: apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, and autophagy-mediated cell death. These processes act as pieces in the mosaic of cardiomyocyte cell death, which come together depending on context and stimulus. This review details each individual process, as well as highlights how they come together to produce various cardiac pathologies. By knowing how the pieces go together we can aim towards the development of efficacious therapeutics, which will enable us to prevent cardiomyocyte loss in the face of stress, both reducing mortality and improving quality of life.
    MeSH term(s) Autophagy/genetics ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Cell Death/genetics ; Ferroptosis/genetics ; Homeostasis/genetics ; Humans ; Mitochondrial Transmembrane Permeability-Driven Necrosis/genetics ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Necroptosis/genetics ; Necrosis/genetics ; Parthanatos/genetics ; Pyroptosis/genetics
    Language English
    Publishing date 2021-10-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2021.166297
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  6. Article: Regulation of cell death in the cardiovascular system.

    Patel, Pooja / Karch, Jason

    International review of cell and molecular biology

    2019  Volume 353, Page(s) 153–209

    Abstract: The adult heart is a post-mitotic terminally differentiated organ; therefore, beyond development, cardiomyocyte cell death is maladaptive. Heart disease is the leading cause of death in the world and aberrant cardiomyocyte cell death is the underlying ... ...

    Abstract The adult heart is a post-mitotic terminally differentiated organ; therefore, beyond development, cardiomyocyte cell death is maladaptive. Heart disease is the leading cause of death in the world and aberrant cardiomyocyte cell death is the underlying problem for most cardiovascular-related diseases and fatalities. In this chapter, we will discuss the different cell death mechanisms that engage during normal cardiac development, aging, and disease states. The most abundant loss of cardiomyocytes occurs during a myocardial infarction, when the blood supply to the heart is obstructed, and the affected myocardium succumbs to cell death. Originally, this form of cell death was considered to be unregulated; however, research from the last half a century clearly demonstrates that this form of cell death is multifaceted and employees various degrees of regulation. We will explore all of the cell death pathways that have been implicated in this disease state and the potential interplay between them. Beyond myocardial infarction, we also explore the role and mechanisms of cardiomyocyte cell death in heart failure, myocarditis, and chemotherapeutic-induced cardiotoxicity. Inhibition of cardiomyocyte cell death has extensive therapeutic potential that will increase the longevity and health of the human heart.
    MeSH term(s) Animals ; Cardiovascular Diseases/pathology ; Cardiovascular System/pathology ; Cell Death ; Heart Neoplasms/drug therapy ; Heart Neoplasms/pathology ; Humans
    Language English
    Publishing date 2019-12-30
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2427220-6
    ISSN 1937-6448 ; 0074-7696
    ISSN 1937-6448 ; 0074-7696
    DOI 10.1016/bs.ircmb.2019.11.005
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  7. Article ; Online: Identity, structure, and function of the mitochondrial permeability transition pore: controversies, consensus, recent advances, and future directions.

    Bernardi, Paolo / Gerle, Christoph / Halestrap, Andrew P / Jonas, Elizabeth A / Karch, Jason / Mnatsakanyan, Nelli / Pavlov, Evgeny / Sheu, Shey-Shing / Soukas, Alexander A

    Cell death and differentiation

    2023  Volume 30, Issue 8, Page(s) 1869–1885

    Abstract: The mitochondrial permeability transition (mPT) describes a ... ...

    Abstract The mitochondrial permeability transition (mPT) describes a Ca
    MeSH term(s) Mitochondrial Permeability Transition Pore/analysis ; Mitochondrial Permeability Transition Pore/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Consensus ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism
    Chemical Substances Mitochondrial Permeability Transition Pore ; Mitochondrial Membrane Transport Proteins
    Language English
    Publishing date 2023-07-17
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-023-01187-0
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  8. Article ; Online: ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy.

    Bround, Michael J / Havens, Julian R / York, Allen J / Sargent, Michelle A / Karch, Jason / Molkentin, Jeffery D

    Science advances

    2023  Volume 9, Issue 34, Page(s) eadi2767

    Abstract: Mitochondrial permeability transition pore (MPTP) formation contributes to ischemia-reperfusion injury in the heart and several degenerative diseases, including muscular dystrophy (MD). MD is a family of genetic disorders characterized by progressive ... ...

    Abstract Mitochondrial permeability transition pore (MPTP) formation contributes to ischemia-reperfusion injury in the heart and several degenerative diseases, including muscular dystrophy (MD). MD is a family of genetic disorders characterized by progressive muscle necrosis and premature death. It has been proposed that the MPTP has two molecular components, the adenine nucleotide translocase (ANT) family of proteins and an unknown component that requires the chaperone cyclophilin D (CypD) to activate. This model was examined in vivo by deleting the gene encoding ANT1 (
    MeSH term(s) Animals ; Mice ; Muscular Dystrophies ; Necrosis ; Cell Death ; Peptidyl-Prolyl Isomerase F ; Disease Models, Animal
    Chemical Substances Peptidyl-Prolyl Isomerase F
    Language English
    Publishing date 2023-08-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adi2767
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  9. Article ; Online: A High-Protein Diet Promotes Atrial Arrhythmogenesis via Absent-in-Melanoma 2 Inflammasome.

    Song, Jia / Wu, Jiao / Robichaux, Dexter J / Li, Tingting / Wang, Shuyue / Arredondo Sancristobal, Maria J / Dong, Bingning / Dobrev, Dobromir / Karch, Jason / Thomas, Sandhya S / Li, Na

    Cells

    2024  Volume 13, Issue 2

    Abstract: High-protein diets (HPDs) offer health benefits, such as weight management and improved metabolic profiles. The effects of HPD on cardiac arrhythmogenesis remain unclear. Atrial fibrillation (AF), the most common arrhythmia, is associated with ... ...

    Abstract High-protein diets (HPDs) offer health benefits, such as weight management and improved metabolic profiles. The effects of HPD on cardiac arrhythmogenesis remain unclear. Atrial fibrillation (AF), the most common arrhythmia, is associated with inflammasome activation. The role of the Absent-in-Melanoma 2 (AIM2) inflammasome in AF pathogenesis remains unexplored. In this study, we discovered that HPD increased susceptibility to AF. To demonstrate the involvement of AIM2 signaling in the pathogenesis of HPD-induced AF, wildtype (WT) and
    MeSH term(s) Animals ; Mice ; Atrial Fibrillation/etiology ; Atrial Fibrillation/metabolism ; Cytoplasm ; Diet, High-Protein/adverse effects ; DNA-Binding Proteins/metabolism ; Inflammasomes
    Chemical Substances Aim2 protein, mouse ; DNA-Binding Proteins ; Inflammasomes
    Language English
    Publishing date 2024-01-05
    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/cells13020108
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  10. Article ; Online: Targeting calcium-mediated inter-organellar crosstalk in cardiac diseases.

    Hulsurkar, Mohit M / Lahiri, Satadru K / Karch, Jason / Wang, Meng C / Wehrens, Xander H T

    Expert opinion on therapeutic targets

    2022  Volume 26, Issue 4, Page(s) 303–317

    Abstract: Introduction: Abnormal calcium signaling between organelles such as the sarcoplasmic reticulum (SR), mitochondria and lysosomes is a key feature of heart diseases. Calcium serves as a secondary messenger mediating inter-organellar crosstalk, essential ... ...

    Abstract Introduction: Abnormal calcium signaling between organelles such as the sarcoplasmic reticulum (SR), mitochondria and lysosomes is a key feature of heart diseases. Calcium serves as a secondary messenger mediating inter-organellar crosstalk, essential for maintaining the cardiomyocyte function.
    Areas covered: This article examines the available literature related to calcium channels and transporters involved in inter-organellar calcium signaling. The SR calcium-release channels ryanodine receptor type-2 (RyR2) and inositol 1,4,5-trisphosphate receptor (IP
    Expert opinion: Enhanced SR calcium release via RyR2 and reduced SR reuptake via SERCA2a, increased VDAC and MCUC-mediated calcium uptake into mitochondria, and enhanced lysosomal calcium-release via lysosomal TPC and TRPML may all contribute to aberrant calcium homeostasis causing heart disease. While mechanisms of this crosstalk need to be studied further, interventions targeting these calcium channels or combinations thereof might represent a promising therapeutic strategy.
    MeSH term(s) Calcium/metabolism ; Calcium Signaling ; Heart Diseases/metabolism ; Humans ; Myocytes, Cardiac/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism
    Chemical Substances Ryanodine Receptor Calcium Release Channel ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-04-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2022.2067479
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