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  1. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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  2. Article: The Small GTPase Rab7 Regulates Release of Mitochondria in Extracellular Vesicles in Response to Lysosomal Dysfunction.

    Liang, Wenjing / Diao, Rachel Y / Quiles, Justin M / Najor, Rita H / Chi, Liguo / Woodall, Benjamin P / Leon, Leonardo J / Duran, Jason / Cauvi, David M / De Maio, Antonio / Adler, Eric D / Gustafsson, Ã Sa B

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways ...

    Abstract Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways that converge on the lysosome. Here, we identified an alternative mechanism to eliminate mitochondria when lysosomal function is compromised. We show that lysosomal inhibition leads to increased secretion of mitochondria in large extracellular vesicles (EVs). The EVs are produced in multivesicular bodies, and their release is independent of autophagy. Deletion of the small GTPase Rab7 in cells or adult mouse heart leads to increased secretion of EVs containing ubiquitinated cargos, including intact mitochondria. The secreted EVs are captured by macrophages without activating inflammation. Hearts from aged mice or Danon disease patients have increased levels of secreted EVs containing mitochondria indicating activation of vesicular release during cardiac pathophysiology. Overall, these findings establish that mitochondria are eliminated in large EVs through the endosomal pathway when lysosomal degradation is inhibited.
    Language English
    Publishing date 2023-02-13
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.02.11.528148
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Deciphering functional roles and interplay between Beclin1 and Beclin2 in autophagosome formation and mitophagy.

    Quiles, Justin M / Najor, Rita H / Gonzalez, Eileen / Jeung, Monica / Liang, Wenjing / Burbach, Sarah M / Zumaya, Erika A / Diao, Rachel Y / Lampert, Mark A / Gustafsson, Åsa B

    Science signaling

    2023  Volume 16, Issue 770, Page(s) eabo4457

    Abstract: The degradation of macromolecules and organelles by the process of autophagy is critical for cellular homeostasis and is often compromised during aging and disease. Beclin1 and Beclin2 are implicated in autophagy induction, and these homologs share a ... ...

    Abstract The degradation of macromolecules and organelles by the process of autophagy is critical for cellular homeostasis and is often compromised during aging and disease. Beclin1 and Beclin2 are implicated in autophagy induction, and these homologs share a high degree of amino acid sequence similarity but have divergent N-terminal regions. Here, we investigated the functions of the Beclin homologs in regulating autophagy and mitophagy, a specialized form of autophagy that targets mitochondria. Both Beclin homologs contributed to autophagosome formation, but a mechanism of autophagosome formation independent of either Beclin homolog occurred in response to starvation or mitochondrial damage. Mitophagy was compromised only in Beclin1-deficient HeLa cells and mouse embryonic fibroblasts because of defective autophagosomal engulfment of mitochondria, and the function of Beclin1 in mitophagy required the phosphorylation of the conserved Ser
    MeSH term(s) Animals ; Humans ; Mice ; Autophagosomes/metabolism ; Autophagy ; Beclin-1/genetics ; Beclin-1/metabolism ; Fibroblasts/metabolism ; HeLa Cells ; Mitophagy
    Chemical Substances Beclin-1 ; Becn2 protein, mouse
    Language English
    Publishing date 2023-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abo4457
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitochondria are secreted in extracellular vesicles when lysosomal function is impaired.

    Liang, Wenjing / Sagar, Shakti / Ravindran, Rishith / Najor, Rita H / Quiles, Justin M / Chi, Liguo / Diao, Rachel Y / Woodall, Benjamin P / Leon, Leonardo J / Zumaya, Erika / Duran, Jason / Cauvi, David M / De Maio, Antonio / Adler, Eric D / Gustafsson, Åsa B

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 5031

    Abstract: Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways ...

    Abstract Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways that converge on the lysosome. Here, we identified an alternative mechanism to eliminate mitochondria when lysosomal function is compromised. We show that lysosomal inhibition leads to increased secretion of mitochondria in large extracellular vesicles (EVs). The EVs are produced in multivesicular bodies, and their release is independent of autophagy. Deletion of the small GTPase Rab7 in cells or adult mouse heart leads to increased secretion of EVs containing ubiquitinated cargos, including intact mitochondria. The secreted EVs are captured by macrophages without activating inflammation. Hearts from aged mice or Danon disease patients have increased levels of secreted EVs containing mitochondria indicating activation of vesicular release during cardiac pathophysiology. Overall, these findings establish that mitochondria are eliminated in large EVs through the endosomal pathway when lysosomal degradation is inhibited.
    MeSH term(s) Animals ; Mice ; Lysosomes ; Mitochondria ; Biological Transport ; Extracellular Vesicles ; Multivesicular Bodies
    Language English
    Publishing date 2023-08-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-40680-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Aging is associated with a decline in Atg9b-mediated autophagosome formation and appearance of enlarged mitochondria in the heart.

    Liang, Wenjing / Moyzis, Alexandra G / Lampert, Mark A / Diao, Rachel Y / Najor, Rita H / Gustafsson, Åsa B

    Aging cell

    2020  Volume 19, Issue 8, Page(s) e13187

    Abstract: Advancing age is a major risk factor for developing heart disease, and the biological processes contributing to aging are currently under intense investigation. Autophagy is an important cellular quality control mechanism that is reduced in tissues with ... ...

    Abstract Advancing age is a major risk factor for developing heart disease, and the biological processes contributing to aging are currently under intense investigation. Autophagy is an important cellular quality control mechanism that is reduced in tissues with age but the molecular mechanisms underlying the age-associated defects in autophagy remain poorly characterized. Here, we have investigated how the autophagic process is altered in aged mouse hearts. We report that autophagic activity is reduced in aged hearts due to a reduction in autophagosome formation. Gene expression profile analysis to evaluate changes in autophagy regulators uncovered a reduction in Atg9b transcript and protein levels. Atg9 proteins are critical in delivering membrane to the growing autophagosome, and siRNA knockdown of Atg9b in cells confirmed a reduction in autophagosome formation. Autophagy is also the main pathway involved in eliminating dysfunctional mitochondria via a process known as mitophagy. The E3 ubiquitin ligase Parkin plays a key role in labeling mitochondria for mitophagy. We also found increased levels of Parkin-positive mitochondria in the aged hearts, an indication that they have been labeled for mitophagy. In contrast, Nrf1, a major transcriptional regulator of mitochondrial biogenesis, was significantly reduced in aged hearts. Additionally, our data showed reduced Drp1-mediated mitochondrial fission and formation of enlarged mitochondria in the aged heart. Overall, our findings suggest that cardiac aging is associated with reduced autophagosome number, decreased mitochondrial turnover, and formation of megamitochondria.
    MeSH term(s) Aging/physiology ; Animals ; Autophagosomes/metabolism ; Autophagosomes/physiology ; Autophagy/physiology ; Autophagy-Related Proteins/metabolism ; HeLa Cells ; Heart/physiology ; Humans ; Male ; Membrane Proteins/metabolism ; Mice ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/physiology ; Myocardium/cytology ; Myocardium/metabolism
    Chemical Substances ATG9B protein, human ; Atg9b protein, mouse ; Autophagy-Related Proteins ; Membrane Proteins
    Language English
    Publishing date 2020-07-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13187
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6581: Show issues Location:
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  6. Article ; Online: SIRT1 accelerates the progression of activity-based anorexia.

    Robinette, Timothy M / Nicholatos, Justin W / Francisco, Adam B / Brooks, Kayla E / Diao, Rachel Y / Sorbi, Sandro / Ricca, Valdo / Nacmias, Benedetta / Brieño-Enríquez, Miguel A / Libert, Sergiy

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 2814

    Abstract: Food consumption is fundamental for life, and eating disorders often result in devastating or life-threatening conditions. Anorexia nervosa (AN) is characterized by a persistent restriction of energy intake, leading to lowered body weight, constant fear ... ...

    Abstract Food consumption is fundamental for life, and eating disorders often result in devastating or life-threatening conditions. Anorexia nervosa (AN) is characterized by a persistent restriction of energy intake, leading to lowered body weight, constant fear of gaining weight, and psychological disturbances of body perception. Herein, we demonstrate that SIRT1 inhibition, both genetically and pharmacologically, delays the onset and progression of AN behaviors in activity-based anorexia (ABA) models, while SIRT1 activation accelerates ABA phenotypes. Mechanistically, we suggest that SIRT1 promotes progression of ABA, in part through its interaction with NRF1, leading to suppression of a NMDA receptor subunit Grin2A. Our results suggest that AN may arise from pathological positive feedback loops: voluntary food restriction activates SIRT1, promoting anxiety, hyperactivity, and addiction to starvation, exacerbating the dieting and exercising, thus further activating SIRT1. We propose SIRT1 inhibition can break this cycle and provide a potential therapy for individuals suffering from AN.
    MeSH term(s) Animals ; Anorexia Nervosa/metabolism ; Body Weight ; Carbazoles/pharmacology ; Disease Models, Animal ; Female ; Gene Expression Regulation ; Heterocyclic Compounds, 4 or More Rings/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/metabolism ; Nuclear Respiratory Factor 1/metabolism ; Phenotype ; Receptors, N-Methyl-D-Aspartate/metabolism ; Resveratrol/pharmacology ; Sirtuin 1/metabolism ; Stress, Mechanical ; Up-Regulation
    Chemical Substances 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide ; Carbazoles ; Gprin1 protein, mouse ; Heterocyclic Compounds, 4 or More Rings ; Nerve Tissue Proteins ; Nrf1 protein, mouse ; Nuclear Respiratory Factor 1 ; Receptors, N-Methyl-D-Aspartate ; SRT1720 ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Resveratrol (Q369O8926L) ; N-methyl D-aspartate receptor subtype 2A (VH92ICR8HX)
    Language English
    Publishing date 2020-06-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-16348-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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