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  1. Article ; Online: Cardiovascular aging: the mitochondrial influence.

    Sagar, Shakti / Gustafsson, Asa B

    The journal of cardiovascular aging

    2023  Volume 3, Issue 3

    Abstract: Age-associated cardiovascular disease is becoming progressively prevalent due to the increased lifespan of the population. However, the fundamental mechanisms underlying the aging process and the corresponding decline in tissue functions are still poorly ...

    Abstract Age-associated cardiovascular disease is becoming progressively prevalent due to the increased lifespan of the population. However, the fundamental mechanisms underlying the aging process and the corresponding decline in tissue functions are still poorly understood. The heart has a very high energy demand and the cellular energy needed to sustain contraction is primarily generated by mitochondrial oxidative phosphorylation. Mitochondria are also involved in supporting various metabolic processes, as well as activation of the innate immune response and cell death pathways. Given the central role of mitochondria in energy metabolism and cell survival, the heart is highly susceptible to the effects of mitochondrial dysfunction. These key organelles have been implicated as underlying drivers of cardiac aging. Here, we review the evidence demonstrating the mitochondrial contribution to the cardiac aging process and disease susceptibility. We also discuss the potential mechanisms responsible for the age-related decline in mitochondrial function.
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Journal Article
    ISSN 2768-5993
    ISSN (online) 2768-5993
    DOI 10.20517/jca.2023.22
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  2. Article ; Online: DRP1-Mediated Mitophagy: Safeguarding Obese Hearts From Cardiomyopathy.

    Fang, Xi / Gustafsson, Åsa B

    Circulation research

    2023  Volume 133, Issue 1, Page(s) 22–24

    MeSH term(s) Humans ; Mitophagy ; Cardiomyopathies ; Heart ; Dynamins ; Mitochondrial Dynamics
    Chemical Substances Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2023-06-22
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323013
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  3. Article ; Online: Passing the βAR: PI3Kγ Is the Judge of β Adrenergic Receptor Resensitization.

    Quiles, Justin M / Gustafsson, Åsa B

    Circulation research

    2023  Volume 132, Issue 6, Page(s) 704–706

    MeSH term(s) Receptors, Adrenergic, beta ; Receptors, Adrenergic, beta-2
    Chemical Substances Receptors, Adrenergic, beta ; Receptors, Adrenergic, beta-2
    Language English
    Publishing date 2023-03-16
    Publishing country United States
    Document type Editorial ; 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.123.322554
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  4. Article ; Online: Protocol to separate small and large extracellular vesicles from mouse and human cardiac tissues.

    Liang, Wenjing / Najor, Rita H / Gustafsson, Åsa B

    STAR protocols

    2024  Volume 5, Issue 1, Page(s) 102914

    Abstract: Extracellular vesicles (EVs) are secreted by cells under various conditions and can contribute to the disease progression in tissues. Here, we present a protocol to separate small and large EVs from mouse hearts and cardiac tissues collected from ... ...

    Abstract Extracellular vesicles (EVs) are secreted by cells under various conditions and can contribute to the disease progression in tissues. Here, we present a protocol to separate small and large EVs from mouse hearts and cardiac tissues collected from patients. We describe steps for utilizing enzymatic digestion for release of EVs from interstitial space followed by differential centrifugation and immunoaffinity purification. The isolated EVs can be used for various experiments to gain insight into their in vivo functions. For complete details on the use and execution of this protocol, please refer to Liang et al. (2023).
    MeSH term(s) Humans ; Mice ; Animals ; Extracellular Vesicles ; Heart ; Centrifugation
    Language English
    Publishing date 2024-02-21
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2024.102914
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  5. Article ; Online: Autophagy: A savior in cigarette smoke-induced cardiac injury.

    Gustafsson, Åsa B

    Journal of molecular and cellular cardiology

    2020  Volume 148, Page(s) 120–121

    MeSH term(s) Animals ; Autophagy ; Beclin-1/metabolism ; Heart Injuries/etiology ; Heart Injuries/pathology ; Mice ; Mitochondria/metabolism ; Mitochondria/pathology ; Smoking/adverse effects
    Chemical Substances Beclin-1
    Language English
    Publishing date 2020-09-10
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2020.09.002
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  6. Article ; Online: The role of mitochondrial fission in cardiovascular health and disease.

    Quiles, Justin M / Gustafsson, Åsa B

    Nature reviews. Cardiology

    2022  Volume 19, Issue 11, Page(s) 723–736

    Abstract: Mitochondria are organelles involved in the regulation of various important cellular processes, ranging from ATP generation to immune activation. A healthy mitochondrial network is essential for cardiovascular function and adaptation to pathological ... ...

    Abstract Mitochondria are organelles involved in the regulation of various important cellular processes, ranging from ATP generation to immune activation. A healthy mitochondrial network is essential for cardiovascular function and adaptation to pathological stressors. Mitochondria undergo fission or fusion in response to various environmental cues, and these dynamic changes are vital for mitochondrial function and health. In particular, mitochondrial fission is closely coordinated with the cell cycle and is linked to changes in mitochondrial respiration and membrane permeability. Another key function of fission is the segregation of damaged mitochondrial components for degradation by mitochondrial autophagy (mitophagy). Mitochondrial fission is induced by the large GTPase dynamin-related protein 1 (DRP1) and is subject to sophisticated regulation. Activation requires various post-translational modifications of DRP1, actin polymerization and the involvement of other organelles such as the endoplasmic reticulum, Golgi apparatus and lysosomes. A decrease in mitochondrial fusion can also shift the balance towards mitochondrial fission. Although mitochondrial fission is necessary for cellular homeostasis, this process is often aberrantly activated in cardiovascular disease. Indeed, strong evidence exists that abnormal mitochondrial fission directly contributes to disease development. In this Review, we compare the physiological and pathophysiological roles of mitochondrial fission and discuss the therapeutic potential of preventing excessive mitochondrial fission in the heart and vasculature.
    MeSH term(s) Actins ; Adenosine Triphosphate ; Dynamins/metabolism ; GTP Phosphohydrolases/metabolism ; Humans ; Mitochondrial Dynamics/physiology
    Chemical Substances Actins ; Adenosine Triphosphate (8L70Q75FXE) ; GTP Phosphohydrolases (EC 3.6.1.-) ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2022-05-06
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-022-00703-y
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  7. Article ; Online: Temporal Effects of Safflower Oil Diet-Based Linoleic Acid Supplementation on Barth Syndrome Cardiomyopathy.

    Zhu, Siting / Pang, Jing / Nguyen, Anh / Tan, Changming / Tso, Alexandria / Huynh, Tiana / Gu, Yusu / Gustafsson, Asa B / Vaz, Frédéric M / Evans, Sylvia M / Fang, Xi

    Circulation

    2024  Volume 149, Issue 10, Page(s) 790–793

    MeSH term(s) Humans ; Linoleic Acid ; Safflower Oil ; Barth Syndrome ; Diet ; Dietary Supplements/adverse effects
    Chemical Substances Linoleic Acid (9KJL21T0QJ) ; Safflower Oil (8001-23-8)
    Language English
    Publishing date 2024-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.123.065414
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  8. Article ; Online: Mitochondrial quality surveillance: mitophagy in cardiovascular health and disease.

    Diao, Rachel Y / Gustafsson, Åsa B

    American journal of physiology. Cell physiology

    2021  Volume 322, Issue 2, Page(s) C218–C230

    Abstract: Selective autophagy of mitochondria, known as mitophagy, is a major quality control pathway in the heart that is involved in removing unwanted or dysfunctional mitochondria from the cell. Baseline mitophagy is critical for maintaining fitness of the ... ...

    Abstract Selective autophagy of mitochondria, known as mitophagy, is a major quality control pathway in the heart that is involved in removing unwanted or dysfunctional mitochondria from the cell. Baseline mitophagy is critical for maintaining fitness of the mitochondrial network by continuous turnover of aged and less-functional mitochondria. Mitophagy is also critical in adapting to stress associated with mitochondrial damage or dysfunction. The removal of damaged mitochondria prevents reactive oxygen species-mediated damage to proteins and DNA and suppresses activation of inflammation and cell death. Impairments in mitophagy are associated with the pathogenesis of many diseases, including cancers, inflammatory diseases, neurodegeneration, and cardiovascular disease. Mitophagy is a highly regulated and complex process that requires the coordination of labeling dysfunctional mitochondria for degradation while simultaneously promoting de novo autophagosome biogenesis adjacent to the cargo. In this review, we provide an update on our current understanding of these steps in mitophagy induction and discuss the physiological and pathophysiological consequences of altered mitophagy in the heart.
    MeSH term(s) Animals ; COVID-19/metabolism ; COVID-19/pathology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitophagy/physiology ; Phagocytosis/physiology ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2021-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00360.2021
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  9. Article: Mitochondrial Quality Control and Cellular Proteostasis: Two Sides of the Same Coin.

    Quiles, Justin M / Gustafsson, Åsa B

    Frontiers in physiology

    2020  Volume 11, Page(s) 515

    Abstract: Mitochondrial dysfunction is a hallmark of cardiac pathophysiology. Defects in mitochondrial performance disrupt contractile function, overwhelm myocytes with reactive oxygen species (ROS), and transform these cellular powerhouses into pro-death ... ...

    Abstract Mitochondrial dysfunction is a hallmark of cardiac pathophysiology. Defects in mitochondrial performance disrupt contractile function, overwhelm myocytes with reactive oxygen species (ROS), and transform these cellular powerhouses into pro-death organelles. Thus, quality control (QC) pathways aimed at identifying and removing damaged mitochondrial proteins, components, or entire mitochondria are crucial processes in post-mitotic cells such as cardiac myocytes. Almost all of the mitochondrial proteins are encoded by the nuclear genome and the trafficking of these nuclear-encoded proteins necessitates significant cross-talk with the cytosolic protein QC machinery to ensure that only functional proteins are delivered to the mitochondria. Within the organelle, mitochondria contain their own protein QC system consisting of chaperones and proteases. This system represents another level of QC to promote mitochondrial protein folding and prevent aggregation. If this system is overwhelmed, a conserved transcriptional response known as the mitochondrial unfolded protein response is activated to increase the expression of proteins involved in restoring mitochondrial proteostasis. If the mitochondrion is beyond repair, the entire organelle must be removed before it becomes cytotoxic and causes cellular damage. Recent evidence has also uncovered mitochondria as participants in cytosolic protein QC where misfolded cytosolic proteins can be imported and degraded inside mitochondria. However, this process also places increased pressure on mitochondrial QC pathways to ensure that the imported proteins do not cause mitochondrial dysfunction. This review is focused on discussing the pathways involved in regulating mitochondrial QC and their relationship to cellular proteostasis and mitochondrial health in the heart.
    Language English
    Publishing date 2020-05-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2020.00515
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  10. Article: The Aging Heart: Mitophagy at the Center of Rejuvenation.

    Liang, Wenjing J / Gustafsson, Åsa B

    Frontiers in cardiovascular medicine

    2020  Volume 7, Page(s) 18

    Abstract: Aging is associated with structural and functional changes in the heart and is a major risk factor in developing cardiovascular disease. Many recent studies have focused on increasing our understanding of the basis of aging at the cellular and molecular ... ...

    Abstract Aging is associated with structural and functional changes in the heart and is a major risk factor in developing cardiovascular disease. Many recent studies have focused on increasing our understanding of the basis of aging at the cellular and molecular levels in various tissues, including the heart. It is known that there is an age-related decline in cellular quality control pathways such as autophagy and mitophagy, which leads to accumulation of potentially harmful cellular components in cardiac myocytes. There is evidence that diminished autophagy and mitophagy accelerate the aging process, while enhancement preserves cardiac homeostasis and extends life span. Here, we review the current knowledge of autophagy and mitophagy in aging and discuss how age-associated alterations in these processes contribute to cardiac aging and age-related cardiovascular diseases.
    Language English
    Publishing date 2020-02-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2020.00018
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