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  1. Article ; Online: From Beats to Metabolism: the Heart at the Core of Interorgan Metabolic Cross Talk.

    Romero-Becera, Rafael / Santamans, Ayelén M / Arcones, Alba C / Sabio, Guadalupe

    Physiology (Bethesda, Md.)

    2023  Volume 39, Issue 2, Page(s) 98–125

    Abstract: The heart, once considered a mere blood pump, is now recognized as a multifunctional metabolic and endocrine organ. Its function is tightly regulated by various metabolic processes, at the same time it serves as an endocrine organ, secreting bioactive ... ...

    Abstract The heart, once considered a mere blood pump, is now recognized as a multifunctional metabolic and endocrine organ. Its function is tightly regulated by various metabolic processes, at the same time it serves as an endocrine organ, secreting bioactive molecules that impact systemic metabolism. In recent years, research has shed light on the intricate interplay between the heart and other metabolic organs, such as adipose tissue, liver, and skeletal muscle. The metabolic flexibility of the heart and its ability to switch between different energy substrates play a crucial role in maintaining cardiac function and overall metabolic homeostasis. Gaining a comprehensive understanding of how metabolic disorders disrupt cardiac metabolism is crucial, as it plays a pivotal role in the development and progression of cardiac diseases. The emerging understanding of the heart as a metabolic and endocrine organ highlights its essential contribution to whole body metabolic regulation and offers new insights into the pathogenesis of metabolic diseases, such as obesity, diabetes, and cardiovascular disorders. In this review, we provide an in-depth exploration of the heart's metabolic and endocrine functions, emphasizing its role in systemic metabolism and the interplay between the heart and other metabolic organs. Furthermore, emerging evidence suggests a correlation between heart disease and other conditions such as aging and cancer, indicating that the metabolic dysfunction observed in these conditions may share common underlying mechanisms. By unraveling the complex mechanisms underlying cardiac metabolism, we aim to contribute to the development of novel therapeutic strategies for metabolic diseases and improve overall cardiovascular health.
    MeSH term(s) Humans ; Diabetes Mellitus/metabolism ; Adipose Tissue/metabolism ; Homeostasis ; Metabolic Diseases/metabolism ; Signal Transduction
    Language English
    Publishing date 2023-12-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00018.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2164: Show issues Location:
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  2. Article ; Online: p38 MAPK Pathway in the Heart: New Insights in Health and Disease.

    Romero-Becerra, Rafael / Santamans, Ayelén M / Folgueira, Cintia / Sabio, Guadalupe

    International journal of molecular sciences

    2020  Volume 21, Issue 19

    Abstract: The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac ... ...

    Abstract The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action in part dependent on the model system under study and the identity of the activated p38 family member. Most studies to date have been performed with inhibitors that are not isoform-specific, and, consequently, knowledge remains very limited about how the different p38s control cardiac physiology and respond to cardiac stress. In this review, we summarize the current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.
    MeSH term(s) Animals ; Arrhythmias, Cardiac/metabolism ; Cardiomegaly/metabolism ; Heart Failure/metabolism ; Humans ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; MAP Kinase Signaling System/drug effects ; Myocardium/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Regeneration/physiology ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Treatment Outcome ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Isoenzymes ; Protein Kinase Inhibitors ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2020-10-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21197412
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: MCJ: A mitochondrial target for cardiac intervention in pulmonary hypertension.

    Santamans, Ayelén M / Cicuéndez, Beatriz / Mora, Alfonso / Villalba-Orero, María / Rajlic, Sanela / Crespo, María / Vo, Paula / Jerome, Madison / Macías, Álvaro / López, Juan Antonio / Leiva, Magdalena / Rocha, Susana F / León, Marta / Rodríguez, Elena / Leiva, Luis / Pintor Chocano, Aránzazu / García Lunar, Inés / García-Álvarez, Ana / Hernansanz-Agustín, Pablo /
    Peinado, Víctor I / Barberá, Joan Albert / Ibañez, Borja / Vázquez, Jesús / Spinelli, Jessica B / Daiber, Andreas / Oliver, Eduardo / Sabio, Guadalupe

    Science advances

    2024  Volume 10, Issue 3, Page(s) eadk6524

    Abstract: Pulmonary hypertension (PH) can affect both pulmonary arterial tree and cardiac function, often leading to right heart failure and death. Despite the urgency, the lack of understanding has limited the development of effective cardiac therapeutic ... ...

    Abstract Pulmonary hypertension (PH) can affect both pulmonary arterial tree and cardiac function, often leading to right heart failure and death. Despite the urgency, the lack of understanding has limited the development of effective cardiac therapeutic strategies. Our research reveals that MCJ modulates mitochondrial response to chronic hypoxia. MCJ levels elevate under hypoxic conditions, as in lungs of patients affected by COPD, mice exposed to hypoxia, and myocardium from pigs subjected to right ventricular (RV) overload. The absence of MCJ preserves RV function, safeguarding against both cardiac and lung remodeling induced by chronic hypoxia. Cardiac-specific silencing is enough to protect against cardiac dysfunction despite the adverse pulmonary remodeling. Mechanistically, the absence of MCJ triggers a protective preconditioning state mediated by the ROS/mTOR/HIF-1α axis. As a result, it preserves RV systolic function following hypoxia exposure. These discoveries provide a potential avenue to alleviate chronic hypoxia-induced PH, highlighting MCJ as a promising target against this condition.
    MeSH term(s) Animals ; Humans ; Mice ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/drug therapy ; Hypoxia ; Lung ; Myocardium ; Pulmonary Artery ; Swine
    Chemical Substances Mcj protein, mouse
    Language English
    Publishing date 2024-01-19
    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.adk6524
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: p38γ and p38δ regulate postnatal cardiac metabolism through glycogen synthase 1.

    Santamans, Ayelén M / Montalvo-Romeral, Valle / Mora, Alfonso / Lopez, Juan Antonio / González-Romero, Francisco / Jimenez-Blasco, Daniel / Rodríguez, Elena / Pintor-Chocano, Aránzazu / Casanueva-Benítez, Cristina / Acín-Pérez, Rebeca / Leiva-Vega, Luis / Duran, Jordi / Guinovart, Joan J / Jiménez-Borreguero, Jesús / Enríquez, José Antonio / Villlalba-Orero, María / Bolaños, Juan P / Aspichueta, Patricia / Vázquez, Jesús /
    González-Terán, Bárbara / Sabio, Guadalupe

    PLoS biology

    2021  Volume 19, Issue 11, Page(s) e3001447

    Abstract: During the first weeks of postnatal heart development, cardiomyocytes undergo a major adaptive metabolic shift from glycolytic energy production to fatty acid oxidation. This metabolic change is contemporaneous to the up-regulation and activation of the ... ...

    Abstract During the first weeks of postnatal heart development, cardiomyocytes undergo a major adaptive metabolic shift from glycolytic energy production to fatty acid oxidation. This metabolic change is contemporaneous to the up-regulation and activation of the p38γ and p38δ stress-activated protein kinases in the heart. We demonstrate that p38γ/δ contribute to the early postnatal cardiac metabolic switch through inhibitory phosphorylation of glycogen synthase 1 (GYS1) and glycogen metabolism inactivation. Premature induction of p38γ/δ activation in cardiomyocytes of newborn mice results in an early GYS1 phosphorylation and inhibition of cardiac glycogen production, triggering an early metabolic shift that induces a deficit in cardiomyocyte fuel supply, leading to whole-body metabolic deregulation and maladaptive cardiac pathogenesis. Notably, the adverse effects of forced premature cardiac p38γ/δ activation in neonate mice are prevented by maternal diet supplementation of fatty acids during pregnancy and lactation. These results suggest that diet interventions have a potential for treating human cardiac genetic diseases that affect heart metabolism.
    MeSH term(s) Animals ; Animals, Newborn ; Cardiomegaly/enzymology ; Cardiomegaly/pathology ; Cardiomegaly/physiopathology ; Diet, High-Fat ; Enzyme Activation ; Feeding Behavior ; Female ; Gene Deletion ; Glucose Intolerance/enzymology ; Glycogen/metabolism ; Glycogen Synthase/metabolism ; Glycogen Synthase Kinase 3/metabolism ; Insulin Resistance ; Lipid Metabolism ; MAP Kinase Signaling System ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 12/metabolism ; Mitogen-Activated Protein Kinase 13/metabolism ; Myocardium/enzymology ; Myocytes, Cardiac/enzymology ; Organ Specificity ; Phosphorylation ; Mice
    Chemical Substances Glycogen (9005-79-2) ; Glycogen Synthase (EC 2.4.1.11) ; Mitogen-Activated Protein Kinase 12 (EC 2.7.1.-) ; Mitogen-Activated Protein Kinase 13 (EC 2.7.1.-) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
    Language English
    Publishing date 2021-11-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.3001447
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6193: Show issues Location:
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  5. Article ; Online: p38α blocks brown adipose tissue thermogenesis through p38δ inhibition.

    Matesanz, Nuria / Nikolic, Ivana / Leiva, Magdalena / Pulgarín-Alfaro, Marta / Santamans, Ayelén M / Bernardo, Edgar / Mora, Alfonso / Herrera-Melle, Leticia / Rodríguez, Elena / Beiroa, Daniel / Caballero, Ainoa / Martín-García, Elena / Acín-Pérez, Rebeca / Hernández-Cosido, Lourdes / Leiva-Vega, Luis / Torres, Jorge L / Centeno, Francisco / Nebreda, Angel R / Enríquez, José Antonio /
    Nogueiras, Rubén / Marcos, Miguel / Sabio, Guadalupe

    PLoS biology

    2018  Volume 16, Issue 7, Page(s) e2004455

    Abstract: Adipose tissue has emerged as an important regulator of whole-body metabolism, and its capacity to dissipate energy in the form of heat has acquired a special relevance in recent years as potential treatment for obesity. In this context, the p38MAPK ... ...

    Abstract Adipose tissue has emerged as an important regulator of whole-body metabolism, and its capacity to dissipate energy in the form of heat has acquired a special relevance in recent years as potential treatment for obesity. In this context, the p38MAPK pathway has arisen as a key player in the thermogenic program because it is required for the activation of brown adipose tissue (BAT) thermogenesis and participates also in the transformation of white adipose tissue (WAT) into BAT-like depot called beige/brite tissue. Here, using mice that are deficient in p38α specifically in adipose tissue (p38αFab-KO), we unexpectedly found that lack of p38α protected against high-fat diet (HFD)-induced obesity. We also showed that p38αFab-KO mice presented higher energy expenditure due to increased BAT thermogenesis. Mechanistically, we found that lack of p38α resulted in the activation of the related protein kinase family member p38δ. Our results showed that p38δ is activated in BAT by cold exposure, and lack of this kinase specifically in adipose tissue (p38δ Fab-KO) resulted in overweight together with reduced energy expenditure and lower body and skin surface temperature in the BAT region. These observations indicate that p38α probably blocks BAT thermogenesis through p38δ inhibition. Consistent with the results obtained in animals, p38α was reduced in visceral and subcutaneous adipose tissue of subjects with obesity and was inversely correlated with body mass index (BMI). Altogether, we have elucidated a mechanism implicated in physiological BAT activation that has potential clinical implications for the treatment of obesity and related diseases such as diabetes.
    MeSH term(s) Adipocytes, Brown/enzymology ; Adipose Tissue, Brown/enzymology ; Adipose Tissue, Brown/physiology ; Adult ; Animals ; Body Mass Index ; Diabetes Mellitus, Experimental/enzymology ; Diabetes Mellitus, Experimental/prevention & control ; Diet ; Energy Metabolism ; Enzyme Activation ; Humans ; MAP Kinase Signaling System ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinase 13/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 13/metabolism ; Mitogen-Activated Protein Kinase 14/metabolism ; Models, Biological ; Obesity/enzymology ; Obesity/prevention & control ; Thermogenesis ; Uncoupling Protein 1/metabolism
    Chemical Substances UCP1 protein, human ; Uncoupling Protein 1 ; Mitogen-Activated Protein Kinase 13 (EC 2.7.1.-) ; Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24)
    Language English
    Publishing date 2018-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.2004455
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  6. Article ; Online: p38γ is essential for cell cycle progression and liver tumorigenesis.

    Tomás-Loba, Antonia / Manieri, Elisa / González-Terán, Bárbara / Mora, Alfonso / Leiva-Vega, Luis / Santamans, Ayelén M / Romero-Becerra, Rafael / Rodríguez, Elena / Pintor-Chocano, Aránzazu / Feixas, Ferran / López, Juan Antonio / Caballero, Beatriz / Trakala, Marianna / Blanco, Óscar / Torres, Jorge L / Hernández-Cosido, Lourdes / Montalvo-Romeral, Valle / Matesanz, Nuria / Roche-Molina, Marta /
    Bernal, Juan Antonio / Mischo, Hannah / León, Marta / Caballero, Ainoa / Miranda-Saavedra, Diego / Ruiz-Cabello, Jesús / Nevzorova, Yulia A / Cubero, Francisco Javier / Bravo, Jerónimo / Vázquez, Jesús / Malumbres, Marcos / Marcos, Miguel / Osuna, Sílvia / Sabio, Guadalupe

    Nature

    2019  Volume 568, Issue 7753, Page(s) 557–560

    Abstract: The cell cycle is a tightly regulated process that is controlled by the conserved cyclin-dependent kinase (CDK)-cyclin protein ... ...

    Abstract The cell cycle is a tightly regulated process that is controlled by the conserved cyclin-dependent kinase (CDK)-cyclin protein complex
    MeSH term(s) Aged ; Animals ; Carcinogenesis/drug effects ; Carcinogenesis/pathology ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/pathology ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Cyclin-Dependent Kinases/metabolism ; Female ; Hepatocytes/cytology ; Hepatocytes/pathology ; Humans ; Liver/enzymology ; Liver/pathology ; Liver/surgery ; Liver Neoplasms/chemically induced ; Liver Neoplasms/enzymology ; Liver Neoplasms/pathology ; Male ; Mice ; Middle Aged ; Mitogen-Activated Protein Kinase 12/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 12/metabolism ; Phosphorylation ; Pyridones/pharmacology ; Retinoblastoma Protein/chemistry ; Retinoblastoma Protein/metabolism ; Sequence Homology ; Substrate Specificity
    Chemical Substances Pyridones ; Retinoblastoma Protein ; pirfenidone (D7NLD2JX7U) ; Mitogen-Activated Protein Kinase 12 (EC 2.7.1.-) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
    Language English
    Publishing date 2019-04-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-019-1112-8
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    Zs.MG 9: Show issues
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