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  1. Article ; Online: Recent advances on the role of monoamine oxidases in cardiac pathophysiology.

    Kaludercic, Nina / Arusei, Ruth Jepchirchir / Di Lisa, Fabio

    Basic research in cardiology

    2023  Volume 118, Issue 1, Page(s) 41

    Abstract: Numerous physiological and pathological roles have been attributed to the formation of mitochondrial reactive oxygen species (ROS). However, the individual contribution of different mitochondrial processes independently of bioenergetics remains elusive ... ...

    Abstract Numerous physiological and pathological roles have been attributed to the formation of mitochondrial reactive oxygen species (ROS). However, the individual contribution of different mitochondrial processes independently of bioenergetics remains elusive and clinical treatments unavailable. A notable exception to this complexity is found in the case of monoamine oxidases (MAOs). Unlike other ROS-producing enzymes, especially within mitochondria, MAOs possess a distinct combination of defined molecular structure, substrate specificity, and clinically accessible inhibitors. Another significant aspect of MAO activity is the simultaneous generation of hydrogen peroxide alongside highly reactive aldehydes and ammonia. These three products synergistically impair mitochondrial function at various levels, ultimately jeopardizing cellular metabolic integrity and viability. This pathological condition arises from exacerbated MAO activity, observed in many cardiovascular diseases, thus justifying the exploration of MAO inhibitors as effective cardioprotective strategy. In this context, we not only summarize the deleterious roles of MAOs in cardiac pathologies and the positive effects resulting from genetic or pharmacological MAO inhibition, but also discuss recent findings that expand our understanding on the role of MAO in gene expression and cardiac development.
    MeSH term(s) Humans ; Monoamine Oxidase/genetics ; Monoamine Oxidase/metabolism ; Reactive Oxygen Species/metabolism ; Oxidative Stress/physiology ; Heart ; Cardiovascular Diseases
    Chemical Substances Monoamine Oxidase (EC 1.4.3.4) ; Reactive Oxygen Species
    Language English
    Publishing date 2023-10-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-023-01012-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: IP

    Rahhali, Karim / Di Lisa, Fabio / Kaludercic, Nina

    Cell calcium

    2023  Volume 110, Page(s) 102700

    Abstract: The close contacts between endoplasmic reticulum and mitochondria (ERMCs) play a key role in metabolic regulation, ... ...

    Abstract The close contacts between endoplasmic reticulum and mitochondria (ERMCs) play a key role in metabolic regulation, Ca
    MeSH term(s) Calcium Signaling/physiology ; Mitochondria/metabolism ; Homeostasis/physiology ; Calcium/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-01-25
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2023.102700
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cyclophilin D and p66Shc contribute to KCl-induced Ca2+ increase in pulmonary artery smooth muscle cells: a potentially relevant phenomenon awaiting a definite mechanism.

    Kaludercic, Nina / Di Lisa, Fabio

    Cardiovascular research

    2021  Volume 118, Issue 1, Page(s) 16–17

    MeSH term(s) Calcium/metabolism ; Peptidyl-Prolyl Isomerase F ; Myocytes, Smooth Muscle/metabolism ; Pulmonary Artery/metabolism ; Src Homology 2 Domain-Containing, Transforming Protein 1
    Chemical Substances Peptidyl-Prolyl Isomerase F ; SHC1 protein, human ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-08-03
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvab261
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Editorial: Cardioprotection, sex and gender differences.

    Mercurio, Valentina / Kaludercic, Nina / Paolocci, Nazareno / Penna, Claudia

    Frontiers in physiology

    2022  Volume 13, Page(s) 940058

    Language English
    Publishing date 2022-08-31
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.940058
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Mitochondrial ROS Formation in the Pathogenesis of Diabetic Cardiomyopathy.

    Kaludercic, Nina / Di Lisa, Fabio

    Frontiers in cardiovascular medicine

    2020  Volume 7, Page(s) 12

    Abstract: Diabetic cardiomyopathy is a result of diabetes-induced changes in the structure and function of the heart. Hyperglycemia affects multiple pathways in the diabetic heart, but excessive reactive oxygen species (ROS) generation and oxidative stress ... ...

    Abstract Diabetic cardiomyopathy is a result of diabetes-induced changes in the structure and function of the heart. Hyperglycemia affects multiple pathways in the diabetic heart, but excessive reactive oxygen species (ROS) generation and oxidative stress represent common denominators associated with adverse tissue remodeling. Indeed, key processes underlying cardiac remodeling in diabetes are redox sensitive, including inflammation, organelle dysfunction, alteration in ion homeostasis, cardiomyocyte hypertrophy, apoptosis, fibrosis, and contractile dysfunction. Extensive experimental evidence supports the involvement of mitochondrial ROS formation in the alterations characterizing the diabetic heart. In this review we will outline the central role of mitochondrial ROS and alterations in the redox status contributing to the development of diabetic cardiomyopathy. We will discuss the role of different sources of ROS involved in this process, with a specific emphasis on mitochondrial ROS producing enzymes within cardiomyocytes. Finally, the therapeutic potential of pharmacological inhibitors of ROS sources within the mitochondria will be discussed.
    Language English
    Publishing date 2020-02-18
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2020.00012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The energetic cost of NNT-dependent ROS removal.

    Kaludercic, Nina / Di Lisa, Fabio

    The Journal of biological chemistry

    2020  Volume 295, Issue 48, Page(s) 16217–16218

    Abstract: Under conditions of high nutrient availability and low ATP synthesis, mitochondria generate reactive oxygen species (ROS) that must be removed to avoid cell injury. Among the enzymes involved in this scavenging process, peroxidases play a crucial role, ... ...

    Abstract Under conditions of high nutrient availability and low ATP synthesis, mitochondria generate reactive oxygen species (ROS) that must be removed to avoid cell injury. Among the enzymes involved in this scavenging process, peroxidases play a crucial role, using NADPH provided mostly by nicotinamide nucleotide transhydrogenase (NNT). However, scarce information is available on how and to what extent ROS formation is linked to mitochondrial oxygen consumption. A new study by Smith
    MeSH term(s) Energy Metabolism ; Mitochondria/metabolism ; NADP Transhydrogenases/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Oxygen Species ; NADP Transhydrogenases (EC 1.6.1.-)
    Language English
    Publishing date 2020-11-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.H120.016368
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: MCUB Hearts Mitochondria in Sickness, Less in Health.

    Kaludercic, Nina / Scorrano, Luca

    Circulation

    2019  Volume 140, Issue 21, Page(s) 1734–1736

    MeSH term(s) Calcium ; Calcium Channels ; Mitochondria, Heart
    Chemical Substances Calcium Channels ; mitochondrial calcium uniporter ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2019-11-18
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    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.119.043440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Mitochondrial reactive oxygen species in physiology and disease.

    Antonucci, Salvatore / Di Lisa, Fabio / Kaludercic, Nina

    Cell calcium

    2021  Volume 94, Page(s) 102344

    Abstract: Mitochondrial reactive oxygen species (mROS) are routinely produced at several sites within the organelle. The balance in their formation and elimination is maintained by a complex and robust antioxidant system. mROS may act as second messengers and ... ...

    Abstract Mitochondrial reactive oxygen species (mROS) are routinely produced at several sites within the organelle. The balance in their formation and elimination is maintained by a complex and robust antioxidant system. mROS may act as second messengers and regulate a number of physiological processes, such as insulin signaling, cell differentiation and proliferation, wound healing, etc. Nevertheless, when a sudden or sustained increase in ROS formation is not efficiently neutralized by the endogenous antioxidant defense system, the detrimental impact of high mROS levels on cell function and viability eventually results in disease development. In this review, we will focus on the dual role of mROS in pathophysiology, emphasizing the physiological role exerted by a regulated mROS production/elimination, and discussing the detrimental effects evoked by an imbalance in mitochondrial redox state. Furthermore, we will touch upon the interplay between mROS and Ca
    Language English
    Publishing date 2021-01-02
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2020.102344
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The Dual Function of Reactive Oxygen/Nitrogen Species in Bioenergetics and Cell Death: The Role of ATP Synthase.

    Kaludercic, Nina / Giorgio, Valentina

    Oxidative medicine and cellular longevity

    2016  Volume 2016, Page(s) 3869610

    Abstract: Reactive oxygen species (ROS) and reactive nitrogen species (RNS) targeting mitochondria are major causative factors in disease pathogenesis. The mitochondrial permeability transition pore (PTP) is a mega-channel modulated by calcium and ROS/RNS ... ...

    Abstract Reactive oxygen species (ROS) and reactive nitrogen species (RNS) targeting mitochondria are major causative factors in disease pathogenesis. The mitochondrial permeability transition pore (PTP) is a mega-channel modulated by calcium and ROS/RNS modifications and it has been described to play a crucial role in many pathophysiological events since prolonged channel opening causes cell death. The recent identification that dimers of ATP synthase form the PTP and the fact that posttranslational modifications caused by ROS/RNS also affect cellular bioenergetics through the modulation of ATP synthase catalysis reveal a dual function of these modifications in the cells. Here, we describe mitochondria as a major site of production and as a target of ROS/RNS and discuss the pathophysiological conditions in which oxidative and nitrosative modifications modulate the catalytic and pore-forming activities of ATP synthase.
    MeSH term(s) Animals ; Cell Death/drug effects ; Energy Metabolism/drug effects ; Humans ; Mitochondria/metabolism ; Mitochondrial Proton-Translocating ATPases/physiology ; Oxidation-Reduction ; Reactive Nitrogen Species/pharmacology ; Reactive Nitrogen Species/physiology ; Reactive Oxygen Species/metabolism ; Reactive Oxygen Species/pharmacology
    Chemical Substances Reactive Nitrogen Species ; Reactive Oxygen Species ; Mitochondrial Proton-Translocating ATPases (EC 3.6.3.-)
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1942-0994
    ISSN (online) 1942-0994
    DOI 10.1155/2016/3869610
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Monoamine Oxidase-Dependent Pro-Survival Signaling in Diabetic Hearts Is Mediated by miRNAs.

    Cagnin, Stefano / Brugnaro, Marco / Millino, Caterina / Pacchioni, Beniamina / Troiano, Carmen / Di Sante, Moises / Kaludercic, Nina

    Cells

    2022  Volume 11, Issue 17

    Abstract: Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO) inhibition in diabetic cardiomyopathy prevents oxidative stress, mitochondrial and endoplasmic reticulum stress and the ... ...

    Abstract Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO) inhibition in diabetic cardiomyopathy prevents oxidative stress, mitochondrial and endoplasmic reticulum stress and the development of diastolic dysfunction. However, it is unclear whether, in addition to the direct effects exerted on the mitochondria, MAO activity is able to post-transcriptionally regulate cardiomyocyte function and survival in diabetes. To this aim, we performed gene and miRNA expression profiling in cardiac tissue from streptozotocin-treated mice (model of type 1 diabetes (T1D)), administered with either vehicle or MAOs inhibitor pargyline for 12 weeks. We found that inhibition of MAO activity in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts increased miR-133a-3p, -193a-3p and -27a-3p expression. These miRNAs target insulin-like growth factor receptor 1 (
    MeSH term(s) Animals ; Diabetes Mellitus, Type 1 ; Diabetic Cardiomyopathies/genetics ; Diabetic Cardiomyopathies/metabolism ; Mice ; MicroRNAs/genetics ; Monoamine Oxidase/genetics ; Monoamine Oxidase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction
    Chemical Substances MicroRNAs ; Reactive Oxygen Species ; Monoamine Oxidase (EC 1.4.3.4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2022-08-30
    Publishing country Switzerland
    Document type Journal Article ; 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/cells11172697
    Database MEDical Literature Analysis and Retrieval System OnLINE

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