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Article ; Online: Lithium downregulates phosphorylated acetyl‑CoA carboxylase 2 and attenuates mitochondrial fatty acid utilization and oxidative stress in cardiomyocytes.

Chen, Pao-Huan / Lee, Ting-Wei / Liu, Shuen-Hsin / Huynh, Tin Van / Chung, Cheng-Chih / Yeh, Yung-Hsin / Kao, Yu-Hsun / Chen, Yi-Jen

Experimental and therapeutic medicine

2024 Volume 27, Issue 4, Page(s) 126

Abstract: Acetyl-CoA carboxylase 2 plays a crucial role in regulating mitochondrial fatty acid oxidation in cardiomyocytes. Lithium, a monovalent cation known for its cardioprotective potential, has been investigated for its influence on mitochondrial ... ...

Abstract	Acetyl-CoA carboxylase 2 plays a crucial role in regulating mitochondrial fatty acid oxidation in cardiomyocytes. Lithium, a monovalent cation known for its cardioprotective potential, has been investigated for its influence on mitochondrial bioenergetics. The present study explored whether lithium modulated acetyl-CoA carboxylase 2 and mitochondrial fatty acid metabolism in cardiomyocytes and the potential therapeutic applications of lithium in alleviating metabolic stress. Mitochondrial bioenergetic function, fatty acid oxidation, reactive oxygen species production, membrane potential and the expression of proteins involved in fatty acid metabolism in H9c2 cardiomyocytes treated with LiCl for 48 h was measured by using a Seahorse extracellular flux analyzer, fluorescence microscopy and western blotting. Small interfering RNA against glucose transporter type 4 was transfected into H9c2 cardiomyocytes for 48 h to induce metabolic stress mimicking insulin resistance. The results revealed that LiCl at a concentration of 0.3 mM (but not at a concentration of 0.1 or 1.0 mM) upregulated the expression of phosphorylated (p-)glycogen synthase kinase-3 beta and downregulated the expression of p-acetyl-CoA carboxylase 2 but did not affect the expression of adenosine monophosphate-activated protein kinase or calcineurin. Cotreatment with TWS119 (8 µM) and LiCl (0.3 mM) downregulated p-acetyl-CoA carboxylase 2 expression to a similar extent as did treatment with TWS119 (8 µM) alone. Moreover, LiCl (0.3 mM) inhibited mitochondrial fatty acid oxidation, improved coupling efficiency and the cellular respiratory control ratio, hindered reactive oxygen species production and proton leakage and restored mitochondrial membrane potential in glucose transporter type 4 knockdown-H9c2 cardiomyocytes. These findings suggested that low therapeutic levels of lithium can downregulate p-acetyl-CoA carboxylase 2, thus reducing mitochondrial fatty acid oxidation and oxidative stress in cardiomyocytes.
Language	English
Publishing date	2024-02-05
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2024.12413
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Article: Editorial: Transcription factors and arrhythmogenesis.

Kao, Yu-Hsun / Chen, Yi-Jen / Higa, Satoshi / Chattipakorn, Nipon / Santulli, Gaetano

Frontiers in physiology

2023 Volume 14, Page(s) 1169747

Language	English
Publishing date	2023-02-28
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1169747
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Article ; Online: Spike Protein Impairs Mitochondrial Function in Human Cardiomyocytes: Mechanisms Underlying Cardiac Injury in COVID-19.

Huynh, Tin Van / Rethi, Lekha / Lee, Ting-Wei / Higa, Satoshi / Kao, Yu-Hsun / Chen, Yi-Jen

Cells

2023 Volume 12, Issue 6

Abstract: Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key ... ...

Abstract	Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key heart functions. We hypothesized that S1 would directly impair the functions of cardiomyocyte mitochondria, thus causing cardiac dysfunction. Methods: Through the Seahorse Mito Stress Test and real-time ATP rate assays, we explored the mitochondrial bioenergetics in human cardiomyocytes (AC16). The cells were treated without (control) or with S1 (1 nM) for 24, 48, and 72 h and we observed the mitochondrial morphology using transmission electron microscopy and confocal fluorescence microscopy. Western blotting, XRhod-1, and MitoSOX Red staining were performed to evaluate the expression of proteins related to energetic metabolism and relevant signaling cascades, mitochondrial Ca Results: The 24 h S1 treatment increased ATP production and mitochondrial respiration by increasing the expression of fatty-acid-transporting regulators and inducing more negative mitochondrial membrane potential (Δψm). The 72 h S1 treatment decreased mitochondrial respiration rates and Δψm, but increased levels of reactive oxygen species (ROS), mCa Conclusion: S1 might impair mitochondrial function in human cardiomyocytes by altering Δψm, mCa
MeSH term(s)	Rats ; Animals ; Humans ; Myocytes, Cardiac/metabolism ; Reactive Oxygen Species/metabolism ; Rats, Sprague-Dawley ; Angiotensin-Converting Enzyme 2/metabolism ; Spike Glycoprotein, Coronavirus/metabolism ; COVID-19/metabolism ; SARS-CoV-2/metabolism ; Mitochondria, Heart/metabolism ; Adenosine Triphosphate/metabolism
Chemical Substances	Reactive Oxygen Species ; spike protein, SARS-CoV-2 ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Spike Glycoprotein, Coronavirus ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2023-03-11
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/cells12060877
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Article: A case of sialolithiasis that mimicked temporomandibular joint disorder.

Kao, Yu-Hsun / Tseng, Chih-Huang / Yu, Chih Kai / Wu, Ju-Hui

Journal of the Formosan Medical Association = Taiwan yi zhi

2022 Volume 121, Issue 10, Page(s) 2135–2137

MeSH term(s)	Humans ; Salivary Gland Calculi/diagnostic imaging ; Temporomandibular Joint ; Temporomandibular Joint Disorders
Language	English
Publishing date	2022-03-01
Publishing country	Singapore
Document type	Case Reports ; Letter
ZDB-ID	2096659-3
ISSN	1876-0821 ; 0929-6646
ISSN (online)	1876-0821
ISSN	0929-6646
DOI	10.1016/j.jfma.2022.02.013
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Article ; Online: Lithium Treatment Improves Cardiac Dysfunction in Rats Deprived of Rapid Eye Movement Sleep.

Chen, Pao-Huan / Chung, Cheng-Chih / Liu, Shuen-Hsin / Kao, Yu-Hsun / Chen, Yi-Jen

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Rapid eye movement (REM) sleep deprivation triggers mania and induces cardiac fibrosis. Beyond neuroprotection, lithium has cardioprotective potential and antifibrotic activity. This study investigated whether lithium improved REM sleep deprivation- ... ...

Abstract	Rapid eye movement (REM) sleep deprivation triggers mania and induces cardiac fibrosis. Beyond neuroprotection, lithium has cardioprotective potential and antifibrotic activity. This study investigated whether lithium improved REM sleep deprivation-induced cardiac dysfunction and evaluated the potential mechanisms. Transthoracic echocardiography, histopathological analysis, and Western blot analysis were performed in control and REM sleep-deprived rats with or without lithium treatment (LiCl of 1 mmol/kg/day administered by oral gavage for 4 weeks) in vivo and in isolated ventricular preparations. The results revealed that REM sleep-deprived rats exhibited impaired contractility and greater fibrosis than control and lithium-treated REM sleep-deprived rats. Western blot analysis showed that REM sleep-deprived hearts had higher expression levels of transforming growth factor beta (TGF-β), phosphorylated Smad 2/3, and alpha-smooth muscle actin than lithium-treated REM sleep-deprived and control hearts. Moreover, lithium-treated REM sleep-deprived hearts had lower expression of angiotensin II type 1 receptor, phosphorylated nuclear factor kappa B p65, calcium release-activated calcium channel protein 1, transient receptor potential canonical (TRPC) 1, and TRPC3 than REM sleep-deprived hearts. The findings suggest that lithium attenuates REM sleep deprivation-induced cardiac fibrogenesis and dysfunction possibly through the downregulation of TGF-β, angiotensin II, and Ca
MeSH term(s)	Actins/metabolism ; Angiotensin II/metabolism ; Animals ; Heart Diseases ; Lithium/pharmacology ; Lithium/therapeutic use ; Lithium Compounds ; NF-kappa B/metabolism ; ORAI1 Protein ; Rats ; Receptor, Angiotensin, Type 1/metabolism ; Sleep Deprivation/complications ; Sleep Deprivation/drug therapy ; Sleep Deprivation/metabolism ; Sleep, REM ; Transforming Growth Factor beta/metabolism
Chemical Substances	Actins ; Lithium Compounds ; NF-kappa B ; ORAI1 Protein ; Receptor, Angiotensin, Type 1 ; Transforming Growth Factor beta ; Angiotensin II (11128-99-7) ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2022-09-23
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/ijms231911226
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Article ; Online: Silicon Oxy-Nitride for the Low Refractive Index Layers in the Mirror Coatings of the Cryogenic Laser Interferometer Gravitational Waves Detector.

Chao, Shiuh / Tsai, Wen-Jie / Tsai, Dong-Lin / Chang, I-Peng / Hong, Qian-Yi / Chang, Wei-Chih / Kao, Yu-Hsun

Physical review letters

2023 Volume 130, Issue 8, Page(s) 81403

Abstract: The low refractive index layers in the mirror coatings of the room-temperature laser interferometer gravitational waves detectors are silica deposited by the ion beam sputter method. However, the silica film suffers from the cryogenic mechanical loss ... ...

Abstract	The low refractive index layers in the mirror coatings of the room-temperature laser interferometer gravitational waves detectors are silica deposited by the ion beam sputter method. However, the silica film suffers from the cryogenic mechanical loss peak, hindering its application for the next generation detector operated at cryogenics. New low refractive index materials need to be explored. We study amorphous silicon oxy-nitride (SiON) films deposited using the method of plasma-enhanced chemical vapor deposition. By changing the N_{2}O/SiH_{4} flow rate ratio, we can tune the refractive index of the SiON smoothly from nitridelike to silicalike of ∼1.48 at 1064 nm, 1550 nm, and 1950 nm. Thermal anneal reduced the refractive index down to ∼1.46 and effectively reduced the absorption and cryogenic mechanical loss; the reductions correlated with the N─H bond concentration decrease. Extinction coefficients of the SiONs at the three wavelengths are reduced down to 5×10^{-6}∼3×10^{-7} by annealing. Cryogenic mechanical losses at 10 K and 20 K (for ET and KAGRA) of the annealed SiONs are significantly lower than the annealed ion beam sputter silica. They are comparable at 120 K (for LIGO-Voyager). Absorption from the vibrational modes of the N─H terminal-hydride structures dominates over the absorption from other terminal hydrides, the Urbach tail, and the silicon dangling bond states in SiON at the three wavelengths.
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.130.081403
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Article ; Online: The Complex Interplay between Imbalanced Mitochondrial Dynamics and Metabolic Disorders in Type 2 Diabetes.

Van Huynh, Tin / Rethi, Lekha / Rethi, Lekshmi / Chen, Chih-Hwa / Chen, Yi-Jen / Kao, Yu-Hsun

Cells

2023 Volume 12, Issue 9

Abstract: Type 2 diabetes mellitus (T2DM) is a global burden, with an increasing number of people affected and increasing treatment costs. The advances in research and guidelines improve the management of blood glucose and related diseases, but T2DM and its ... ...

Abstract	Type 2 diabetes mellitus (T2DM) is a global burden, with an increasing number of people affected and increasing treatment costs. The advances in research and guidelines improve the management of blood glucose and related diseases, but T2DM and its complications are still a big challenge in clinical practice. T2DM is a metabolic disorder in which insulin signaling is impaired from reaching its effectors. Mitochondria are the "powerhouses" that not only generate the energy as adenosine triphosphate (ATP) using pyruvate supplied from glucose, free fatty acid (FFA), and amino acids (AA) but also regulate multiple cellular processes such as calcium homeostasis, redox balance, and apoptosis. Mitochondrial dysfunction leads to various diseases, including cardiovascular diseases, metabolic disorders, and cancer. The mitochondria are highly dynamic in adjusting their functions according to cellular conditions. The shape, morphology, distribution, and number of mitochondria reflect their function through various processes, collectively known as mitochondrial dynamics, including mitochondrial fusion, fission, biogenesis, transport, and mitophagy. These processes determine the overall mitochondrial health and vitality. More evidence supports the idea that dysregulated mitochondrial dynamics play essential roles in the pathophysiology of insulin resistance, obesity, and T2DM, as well as imbalanced mitochondrial dynamics found in T2DM. This review updates and discusses mitochondrial dynamics and the complex interactions between it and metabolic disorders.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/metabolism ; Mitochondrial Dynamics ; Mitochondria/metabolism ; Insulin Resistance ; Insulin/metabolism
Chemical Substances	Insulin
Language	English
Publishing date	2023-04-23
Publishing country	Switzerland
Document type	Journal Article ; Review ; 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/cells12091223
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Article ; Online: Ketogenic Diet Regulates Cardiac Remodeling and Calcium Homeostasis in Diabetic Rat Cardiomyopathy.

Lee, Ting-I / Trang, Nguyen Ngoc / Lee, Ting-Wei / Higa, Satoshi / Kao, Yu-Hsun / Chen, Yao-Chang / Chen, Yi-Jen

International journal of molecular sciences

2023 Volume 24, Issue 22

Abstract: A ketogenic diet (KD) might alleviate patients with diabetic cardiomyopathy. However, the underlying mechanism remains unclear. Myocardial function and arrhythmogenesis are closely linked to calcium ( ... ...

Abstract	A ketogenic diet (KD) might alleviate patients with diabetic cardiomyopathy. However, the underlying mechanism remains unclear. Myocardial function and arrhythmogenesis are closely linked to calcium (Ca
MeSH term(s)	Humans ; Rats ; Male ; Animals ; Calcium/metabolism ; Myocytes, Cardiac/metabolism ; Diabetic Cardiomyopathies/metabolism ; Diet, Ketogenic ; Ventricular Remodeling ; Rats, Wistar ; Ryanodine Receptor Calcium Release Channel/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Sodium/metabolism ; Homeostasis ; Sarcoplasmic Reticulum/metabolism ; Diabetes Mellitus/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Ryanodine Receptor Calcium Release Channel ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2023-11-09
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/ijms242216142
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Article ; Online: Empagliflozin suppressed cardiac fibrogenesis through sodium-hydrogen exchanger inhibition and modulation of the calcium homeostasis.

Chung, Cheng-Chih / Lin, Yung-Kuo / Chen, Yao-Chang / Kao, Yu-Hsun / Yeh, Yung-Hsin / Trang, Nguyen Ngoc / Chen, Yi-Jen

Cardiovascular diabetology

2023 Volume 22, Issue 1, Page(s) 27

Abstract: Background: The novel sodium-glucose co-transporter 2 inhibitor (SGLT2i) potentially ameliorates heart failure and reduces cardiac arrhythmia. Cardiac fibrosis plays a pivotal role in the pathophysiology of HF and atrial myopathy, but the effect of ... ...

Abstract	Background: The novel sodium-glucose co-transporter 2 inhibitor (SGLT2i) potentially ameliorates heart failure and reduces cardiac arrhythmia. Cardiac fibrosis plays a pivotal role in the pathophysiology of HF and atrial myopathy, but the effect of SGLT2i on fibrogenesis remains to be elucidated. This study investigated whether SGLT2i directly modulates fibroblast activities and its underlying mechanisms. Methods and results: Migration, proliferation analyses, intracellular pH assay, intracellular inositol triphosphate (IP3) assay, Ca Conclusions: By inhibiting NHE, empagliflozin decreases the expression of phosphorylated PLC and IP3 production, thereby reducing ER Ca
MeSH term(s)	Rats ; Humans ; Animals ; Calcium/metabolism ; Sodium-Hydrogen Exchangers/metabolism ; Collagen Type I/metabolism ; Atrial Fibrillation ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Homeostasis
Chemical Substances	empagliflozin (HDC1R2M35U) ; Calcium (SY7Q814VUP) ; Sodium-Hydrogen Exchangers ; Collagen Type I ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2023-02-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2093769-6
ISSN	1475-2840 ; 1475-2840
ISSN (online)	1475-2840
ISSN	1475-2840
DOI	10.1186/s12933-023-01756-0
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Article ; Online: Adenosine monophosphate-regulated protein kinase inhibition modulates electrophysiological characteristics and calcium homeostasis of rabbit right ventricular outflow tract.

Lu, Yen-Yu / Cheng, Chen-Chuan / Chen, Yao-Chang / Lin, Yung-Kuo / Higa, Satoshi / Kao, Yu-Hsun / Chen, Yi-Jen

Fundamental & clinical pharmacology

2023 Volume 38, Issue 2, Page(s) 262–275

Abstract: Background: Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate-regulated protein kinase (AMPK) activation is ... ...

Abstract	Background: Metabolic stress predisposes to ventricular arrhythmias and sudden cardiac death. Right ventricular outflow tract (RVOT) is the common origin of ventricular arrhythmias. Adenosine monophosphate-regulated protein kinase (AMPK) activation is an important compensatory mechanism for cardiac remodeling during metabolic stress. Objectives: The purpose of this study was to access whether AMPK inhibition would modulate RVOT electrophysiology, calcium (Ca Methods: Conventional microelectrodes were used to record electrical activity before and after compound C (10 µM, an AMPK inhibitor) in isoproterenol (1 µM)-treated rabbit RVOT tissue preparations under electrical pacing. Whole-cell patch-clamp and confocal microscopic examinations were performed in baseline and compound C-treated rabbit RVOT cardiomyocytes to investigate ionic currents and intracellular Ca Results: Compound C decreased RVOT contractility, and reversed isoproterenol increased RVOT contractility. Compound C decreased the incidence, rate, and duration of isoproterenol-induced RVOT burst firing under rapid pacing. Compared to baseline, compound C-treated RVOT cardiomyocytes had a longer action potential duration, smaller intracellular Ca Conclusion: AMPK inhibition modulates RVOT electrophysiological characteristics and Ca
MeSH term(s)	Animals ; Rabbits ; Calcium/metabolism ; Adenosine Monophosphate ; Isoproterenol/pharmacology ; AMP-Activated Protein Kinases/metabolism ; Arrhythmias, Cardiac/drug therapy ; Myocytes, Cardiac/metabolism ; Homeostasis ; Action Potentials
Chemical Substances	Calcium (SY7Q814VUP) ; Adenosine Monophosphate (415SHH325A) ; Isoproterenol (L628TT009W) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article
ZDB-ID	639134-5
ISSN	1472-8206 ; 0767-3981
ISSN (online)	1472-8206
ISSN	0767-3981
DOI	10.1111/fcp.12953
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