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  1. Article ; Online: Lipotoxicity: a driver of heart failure with preserved ejection fraction?

    Leggat, Jennifer / Bidault, Guillaume / Vidal-Puig, Antonio

    Clinical science (London, England : 1979)

    2021  Volume 135, Issue 19, Page(s) 2265–2283

    Abstract: Heart failure with preserved ejection fraction (HFpEF) is a growing public health concern ... lipid handling, myocardial lipid accumulation and subsequent lipotoxicity. ...

    Abstract Heart failure with preserved ejection fraction (HFpEF) is a growing public health concern, with rising incidence alongside high morbidity and mortality. However, the pathophysiology of HFpEF is not yet fully understood. The association between HFpEF and the metabolic syndrome (MetS) suggests that dysregulated lipid metabolism could drive diastolic dysfunction and subsequent HFpEF. Herein we summarise recent advances regarding the pathogenesis of HFpEF in the context of MetS, with a focus on impaired lipid handling, myocardial lipid accumulation and subsequent lipotoxicity.
    MeSH term(s) Animals ; Cardiometabolic Risk Factors ; Heart Failure/epidemiology ; Heart Failure/metabolism ; Heart Failure/pathology ; Heart Failure/physiopathology ; Humans ; Lipid Metabolism ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/pathology ; Metabolic Syndrome/physiopathology ; Myocardium/metabolism ; Myocardium/pathology ; Prognosis ; Risk Assessment ; Signal Transduction ; Stroke Volume ; Ventricular Function, Left
    Language English
    Publishing date 2021-10-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20210127
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  2. Article ; Online: Heart-Type Fatty Acid Binding Protein Binds Long-Chain Acylcarnitines and Protects against Lipotoxicity.

    Zelencova-Gopejenko, Diana / Videja, Melita / Grandane, Aiga / Pudnika-Okinčica, Linda / Sipola, Anda / Vilks, Karlis / Dambrova, Maija / Jaudzems, Kristaps / Liepinsh, Edgars

    International journal of molecular sciences

    2023  Volume 24, Issue 6

    Abstract: Heart-type fatty-acid binding protein (FABP3) is an essential cytosolic lipid transport protein ...

    Abstract Heart-type fatty-acid binding protein (FABP3) is an essential cytosolic lipid transport protein found in cardiomyocytes. FABP3 binds fatty acids (FAs) reversibly and with high affinity. Acylcarnitines (ACs) are an esterified form of FAs that play an important role in cellular energy metabolism. However, an increased concentration of ACs can exert detrimental effects on cardiac mitochondria and lead to severe cardiac damage. In the present study, we evaluated the ability of FABP3 to bind long-chain ACs (LCACs) and protect cells from their harmful effects. We characterized the novel binding mechanism between FABP3 and LCACs by a cytotoxicity assay, nuclear magnetic resonance, and isothermal titration calorimetry. Our data demonstrate that FABP3 is capable of binding both FAs and LCACs as well as decreasing the cytotoxicity of LCACs. Our findings reveal that LCACs and FAs compete for the binding site of FABP3. Thus, the protective mechanism of FABP3 is found to be concentration dependent.
    MeSH term(s) Fatty Acid Binding Protein 3/metabolism ; Fatty Acid-Binding Proteins/metabolism ; Fatty Acids/pharmacology ; Carnitine ; Myocytes, Cardiac/metabolism
    Chemical Substances acylcarnitine ; Fatty Acid Binding Protein 3 ; Fatty Acid-Binding Proteins ; Fatty Acids ; Carnitine (S7UI8SM58A)
    Language English
    Publishing date 2023-03-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24065528
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  3. Article ; Online: Epicardial adipose tissue and cardiac lipotoxicity: A review.

    Mukherjee, Anirban Goutam / Renu, Kaviyarasi / Gopalakrishnan, Abilash Valsala / Jayaraj, Rama / Dey, Abhijit / Vellingiri, Balachandar / Ganesan, Raja

    Life sciences

    2023  Volume 328, Page(s) 121913

    Abstract: ... clinical processes, epicardial fat can directly impact the heart and coronary arteries by secreting ...

    Abstract Epicardial adipose tissue (EAT) has morphological and physiological contiguity with the myocardium and coronary arteries, making it a visceral fat deposit with some unique properties. Under normal circumstances, EAT exhibits biochemical, mechanical, and thermogenic cardioprotective characteristics. Under clinical processes, epicardial fat can directly impact the heart and coronary arteries by secreting proinflammatory cytokines via vasocrine or paracrine mechanisms. It is still not apparent what factors affect this equilibrium. Returning epicardial fat to its physiological purpose may be possible by enhanced local vascularization, weight loss, and focused pharmacological therapies. This review centers on EAT's developing physiological and pathophysiological dimensions and its various and pioneering clinical utilities.
    MeSH term(s) Pericardium ; Adipose Tissue/physiology ; Myocardium ; Cytokines ; Coronary Vessels
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-07-04
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.121913
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  4. Article ; Online: Lipotoxicity in Kidney, Heart, and Skeletal Muscle Dysfunction.

    Nishi, Hiroshi / Higashihara, Takaaki / Inagi, Reiko

    Nutrients

    2019  Volume 11, Issue 7

    Abstract: ... distribution in the peripheral organs (lipotoxicity), including the kidney, heart, and skeletal muscle ... in the kidney, heart, and skeletal muscle, with the goal of illuminating the nutritional aspects ... of renal dysfunction and even extrarenal complications, including renal anemia, heart failure, and ...

    Abstract Dyslipidemia is a common nutritional and metabolic disorder in patients with chronic kidney disease. Accumulating evidence supports the hypothesis that prolonged metabolic imbalance of lipids leads to ectopic fat distribution in the peripheral organs (lipotoxicity), including the kidney, heart, and skeletal muscle, which accelerates peripheral inflammation and afflictions. Thus, lipotoxicity may partly explain progression of renal dysfunction and even extrarenal complications, including renal anemia, heart failure, and sarcopenia. Additionally, endoplasmic reticulum stress activated by the unfolded protein response pathway plays a pivotal role in lipotoxicity by modulating the expression of key enzymes in lipid synthesis and oxidation. Here, we review the molecular mechanisms underlying lipid deposition and resultant tissue damage in the kidney, heart, and skeletal muscle, with the goal of illuminating the nutritional aspects of these pathologies.
    MeSH term(s) Dyslipidemias/complications ; Heart Diseases/etiology ; Heart Diseases/metabolism ; Humans ; Kidney Diseases/etiology ; Kidney Diseases/metabolism ; Lipid Metabolism ; Muscle, Skeletal/metabolism ; Muscular Diseases/etiology ; Muscular Diseases/metabolism
    Language English
    Publishing date 2019-07-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu11071664
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  5. Article ; Online: Lipotoxicity Disrupts Erythrocyte Function: A Perspective.

    Papadopoulos, Charalampos / Tentes, Ioannis / Anagnostopoulos, Konstantinos

    Cardiovascular & hematological disorders drug targets

    2021  Volume 21, Issue 2, Page(s) 91–94

    Abstract: ... altered in lipotoxic diseases, such as fatty liver disease, heart failure and diabetes. In addition ... causes cell dysfunction, death and inflammation, a biological phenomenon named lipotoxicity. Erythrocytes ... erythrocyte malfunction.: Conclusion: Erythrocytes are an additional cell target of lipotoxicity. Further ...

    Abstract Background: Lipid accumulation in the liver, skeletal and cardiac muscle, kidneys and pancreas causes cell dysfunction, death and inflammation, a biological phenomenon named lipotoxicity. Erythrocytes participate in the transport of lipids in the circulation, and their lipidome is determined by exchange with blood components.
    Objective: The objective of this study is to summarize the current knowledge regarding the effect of toxic lipid accumulation in erythrocytes.
    Results: Erythrocyte lipidome is altered in lipotoxic diseases, such as fatty liver disease, heart failure and diabetes. In addition, ceramide, lysophosphatidylcholine, lysophosphatidic acid, palmitic acid and free cholesterol induce erythrocyte malfunction.
    Conclusion: Erythrocytes are an additional cell target of lipotoxicity. Further exploration of the implicated molecular mechanisms could lead to novel therapeutic targets for cardiometabolic and hematological diseases.
    MeSH term(s) Erythrocytes ; Lipid Metabolism ; Lipids ; Liver ; Myocardium/metabolism
    Chemical Substances Lipids
    Language English
    Publishing date 2021-11-26
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2244164-5
    ISSN 2212-4063 ; 1871-529X
    ISSN (online) 2212-4063
    ISSN 1871-529X
    DOI 10.2174/1871529X21666210719125728
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5610: Show issues Location:
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  6. Book: Glucolipotoxicity and the heart

    Tóth, Peter P. / Raghavan, Vasudevan A.

    (Heart failure clinics ; 8,4)

    2012  

    Author's details guest ed. Peter P. Toth ; Vasudevan A. Raghavan
    Series title Heart failure clinics ; 8,4
    Heart failure clinics
    Collection Heart failure clinics
    Language English
    Size XVIII S., S. 502 - 683 : Ill., graph. Darst.
    Publisher Saunders an imprint of Elsevier
    Publishing place Philadelphia, Pa
    Publishing country United States
    Document type Book
    HBZ-ID HT017472624
    ISBN 978-1-4557-4892-1 ; 1-4557-4892-7
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Zs A 6554 -8,4- verfügbar in Königswinter Königswinter

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  7. Article ; Online: Heart-Type Fatty Acid Binding Protein Binds Long-Chain Acylcarnitines and Protects against Lipotoxicity

    Diana Zelencova-Gopejenko / Melita Videja / Aiga Grandane / Linda Pudnika-Okinčica / Anda Sipola / Karlis Vilks / Maija Dambrova / Kristaps Jaudzems / Edgars Liepinsh

    International Journal of Molecular Sciences, Vol 24, Iss 5528, p

    2023  Volume 5528

    Abstract: Heart-type fatty-acid binding protein (FABP3) is an essential cytosolic lipid transport protein ...

    Abstract Heart-type fatty-acid binding protein (FABP3) is an essential cytosolic lipid transport protein found in cardiomyocytes. FABP3 binds fatty acids (FAs) reversibly and with high affinity. Acylcarnitines (ACs) are an esterified form of FAs that play an important role in cellular energy metabolism. However, an increased concentration of ACs can exert detrimental effects on cardiac mitochondria and lead to severe cardiac damage. In the present study, we evaluated the ability of FABP3 to bind long-chain ACs (LCACs) and protect cells from their harmful effects. We characterized the novel binding mechanism between FABP3 and LCACs by a cytotoxicity assay, nuclear magnetic resonance, and isothermal titration calorimetry. Our data demonstrate that FABP3 is capable of binding both FAs and LCACs as well as decreasing the cytotoxicity of LCACs. Our findings reveal that LCACs and FAs compete for the binding site of FABP3. Thus, the protective mechanism of FABP3 is found to be concentration dependent.
    Keywords long-chain acylcarnitines ; palmitoylcarnitine ; fatty acids ; palmitate ; heart-type fatty acid-binding protein ; FABP3 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: CCDC92 deficiency ameliorates podocyte lipotoxicity in diabetic kidney disease.

    Zuo, Fuwen / Wang, Youzhao / Xu, Xinlei / Ding, Ruihao / Tang, Wei / Sun, Yu / Wang, Xiaojie / Zhang, Yan / Wu, Jichao / Xie, Yusheng / Liu, Min / Wang, Ziying / Yi, Fan

    Metabolism: clinical and experimental

    2023  Volume 150, Page(s) 155724

    Abstract: ... coronary heart disease and type 2 diabetes. However, the expression pattern and role of CCDC92 in the kidney is not clear ... background were generated to clarify the role of CCDC92 in podocyte lipotoxicity.: Results: The level ... promoted podocyte lipotoxicity, at least in part through ABCA1 signaling-mediated lipid homeostasis ...

    Abstract Background and aims: Podocyte injury is considered as the most important early event contributing to diabetic kidney disease (DKD). Recent findings provide new insights into the roles of lipids and lipid-modulating proteins as key determinants of podocyte function in health and kidney disease. CCDC92, a novel member of coiled-coil domain-containing protein family, was indicated relevant to lipid metabolism, coronary heart disease and type 2 diabetes. However, the expression pattern and role of CCDC92 in the kidney is not clear. This study was designed to elucidate the contribution of CCDC92 in the pathogenesis of DKD.
    Methods: Sections with a pathological diagnosis of different classes of DKD, including subjects with mild DKD (class II, n = 6), subjects with moderate DKD (class III, n = 6) or subjects with severe DKD (class IV, n = 6), and control samples (n = 12) were detected for the expression level of CCDC92 and lipid accumulation. Two types of diabetic mice model (db/db and HFD/STZ) in podocyte-specific Ccdc92 knockout background were generated to clarify the role of CCDC92 in podocyte lipotoxicity.
    Results: The level of CCDC92 was increased in renal biopsies sections from patients with DKD, which was correlated with eGFR and lipid accumulation in glomeruli. In animal studies, CCDC92 were also induced in the kidney from two independent diabetic models, especially in podocytes. Podocyte-specific deletion of Ccdc92 ameliorated podocyte injury and ectopic lipid deposition under diabetic condition. Mechanically, CCDC92 promoted podocyte lipotoxicity, at least in part through ABCA1 signaling-mediated lipid homeostasis.
    Conclusion: Our studies demonstrates that CCDC92 acts as a novel regulator of lipid homeostasis to promote podocyte injury in DKD, suggesting that CCDC92 might be a potential biomarker of podocyte injury in DKD, and targeting CCDC92 may be an effective innovative therapeutic strategy for patients with DKD.
    MeSH term(s) Animals ; Humans ; Mice ; Diabetes Mellitus, Experimental/metabolism ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Podocytes/metabolism ; Podocytes/pathology ; Cytoskeletal Proteins/genetics ; Cytoskeletal Proteins/metabolism ; Lipid Metabolism
    Chemical Substances CCDC92 protein, human ; Cytoskeletal Proteins
    Language English
    Publishing date 2023-11-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2023.155724
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  9. Article ; Online: Epicardial adipose tissue and cardiac lipotoxicity: A review

    Mukherjee, Anirban Goutam / Renu, Kaviyarasi / Gopalakrishnan, Abilash Valsala / Jayaraj, Rama / Dey, Abhijit / Vellingiri, Balachandar / Ganesan, Raja

    Life Sciences. 2023 Sept., v. 328 p.121913-

    2023  

    Abstract: ... clinical processes, epicardial fat can directly impact the heart and coronary arteries by secreting ...

    Abstract Epicardial adipose tissue (EAT) has morphological and physiological contiguity with the myocardium and coronary arteries, making it a visceral fat deposit with some unique properties. Under normal circumstances, EAT exhibits biochemical, mechanical, and thermogenic cardioprotective characteristics. Under clinical processes, epicardial fat can directly impact the heart and coronary arteries by secreting proinflammatory cytokines via vasocrine or paracrine mechanisms. It is still not apparent what factors affect this equilibrium. Returning epicardial fat to its physiological purpose may be possible by enhanced local vascularization, weight loss, and focused pharmacological therapies. This review centers on EAT's developing physiological and pathophysiological dimensions and its various and pioneering clinical utilities.
    Keywords adipose tissue ; cytokines ; lipotoxicity ; myocardium ; visceral fat ; weight loss ; Epicardial adipose tissue ; PPAR-γ ; Cardiovascular disease ; Free fatty acids
    Language English
    Dates of publication 2023-09
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.121913
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  10. Article ; Online: Cholesterol 25-hydroxylase prevents type 2 diabetes mellitus induced cardiomyopathy by alleviating cardiac lipotoxicity.

    Zhang, Jialiang / Zhou, Hao / Lei, Fan / Jiang, Kexin / Liao, Yanbiao / Huang, Fangyang / Chen, Mao

    Biochimica et biophysica acta. Molecular basis of disease

    2024  Volume 1870, Issue 5, Page(s) 167158

    Abstract: ... hydroxycholesterol (25HC) were detected in the hearts of T2DM model. Gain- or loss-of-function of CH25H were ... significantly decreased in the hearts of T2DM mice. CH25H: Conclusion: Our study provides compelling evidence ...

    Abstract Objectives: Diabetic cardiomyopathy (DCM) is the leading cause of mortality in type 2 diabetes mellitus (T2DM) patients, with its underlying mechanisms still elusive. This study aims to investigate the role of cholesterol-25-monooxygenase (CH25H) in T2DM induced cardiomyopathy.
    Methods: High fat diet combined with streptozotocin (HFD/STZ) were used to establish a T2DM model. CH25H and its product 25-hydroxycholesterol (25HC) were detected in the hearts of T2DM model. Gain- or loss-of-function of CH25H were performed by receiving AAV9-cTNT-CH25H or CH25H knockout (CH25H
    Results: CH25H and 25HC were significantly decreased in the hearts of T2DM mice. CH25H
    Conclusion: Our study provides compelling evidence supporting the protective role of CH25H in T2DM-induced cardiomyopathy. Furthermore, the regulation of PGC-1α may be intricately involved in this cardioprotective process.
    MeSH term(s) Animals ; Diabetic Cardiomyopathies/metabolism ; Diabetic Cardiomyopathies/pathology ; Diabetic Cardiomyopathies/prevention & control ; Diabetic Cardiomyopathies/etiology ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Mice ; Mice, Knockout ; Male ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Steroid Hydroxylases/metabolism ; Steroid Hydroxylases/genetics ; Diet, High-Fat/adverse effects ; Mice, Inbred C57BL ; Hydroxycholesterols/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics
    Chemical Substances cholesterol 25-hydroxylase ; 25-hydroxycholesterol
    Language English
    Publishing date 2024-04-06
    Publishing country Netherlands
    Document type Journal Article
    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.2024.167158
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