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Article ; Online: Effect of High Sodium Intake on Gut Tight Junctions' Structure and Permeability to Bacterial Toxins in a Rat Model of Chronic Kidney Disease.

Villela-Torres, María de la Luz / Prado-Uribe, María-Del-Carmen / Díaz, Marcela Ávila / Pablo, Héctor Quezada / Soria-Castro, Elizabeth / Escofet, Nuria Esturau / Maldonado, Catalina Elizabeth Flores / Paniagua, Ramón

Archives of medical research

2024 Volume 55, Issue 3, Page(s) 102969

Abstract: Introduction: Uremic toxicity changes the gut structure and permeability, allowing bacterial toxins to translocate from the lumen to the blood during chronic kidney failure (CKD). Clinical fluid overload and tissue edema without uremia have similar ... ...

Abstract	Introduction: Uremic toxicity changes the gut structure and permeability, allowing bacterial toxins to translocate from the lumen to the blood during chronic kidney failure (CKD). Clinical fluid overload and tissue edema without uremia have similar effects but have not been adequately demonstrated and analyzed in CKD. Aims: To investigate the effect of sodium intake on the plasma concentration of gut-derived uremic toxins, indoxyl sulfate (IS), and p-cresyl sulfate (pCS) and the expression of genes and proteins of epithelial gut tight junctions in a rat model of CKD. Methods: Sham-operated (control group, CG) and five-sixths nephrectomized (5/6Nx) Sprague-Dawley rats were randomly assigned to low (LNa), normal (NNa), or high sodium (HNa) diets., Animals were then sacrificed at 8 and 12 weeks and analyzed for IS and pCS plasma concentrations, as well as for gene and protein expression of thigh junction proteins, and transmission electron microscopy (TEM) in colon fragments. Results: The HNa 5/6Nx groups had higher concentrations of IS and pCS than CG, NNa, and LNa at eight and twelve weeks. Furthermore, HNa 5/6Nx groups had reduced expression of the claudin-4 gene and protein than CG, NNa, and LNa. HNa had reduced occludin gene expression compared to CG. Occludin protein expression was more reduced in HNa than in CG, NNa, and LNa. The gut epithelial tight junctions appear dilated in HNa compared to NNa and LNa in TEM. Conclusion: Dietary sodium intake and fluid overload have a significant role in gut epithelial permeability in the CKD model.
MeSH term(s)	Rats ; Animals ; Rats, Sprague-Dawley ; Occludin/genetics ; Occludin/metabolism ; Tight Junctions ; Renal Insufficiency, Chronic ; Bacterial Toxins/metabolism ; Indican ; Sodium, Dietary/metabolism ; Permeability
Chemical Substances	Occludin ; Bacterial Toxins ; Indican (N187WK1Y1J) ; Sodium, Dietary
Language	English
Publishing date	2024-03-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	1156844-6
ISSN	1873-5487 ; 0188-4409 ; 0188-0128
ISSN (online)	1873-5487
ISSN	0188-4409 ; 0188-0128
DOI	10.1016/j.arcmed.2024.102969
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Article ; Online: Redox Homeostasis Alteration Is Restored through Melatonin Treatment in COVID-19 Patients: A Preliminary Study.

Soto, María Elena / Pérez-Torres, Israel / Manzano-Pech, Linaloe / Palacios-Chavarría, Adrían / Valdez-Vázquez, Rafael Ricardo / Guarner-Lans, Verónica / Soria-Castro, Elizabeth / Díaz-Díaz, Eulises / Castrejón-Tellez, Vicente

International journal of molecular sciences

2024 Volume 25, Issue 8

Abstract: Type II pneumocytes are the target of the SARS-CoV-2 virus, which alters their redox homeostasis to increase reactive oxygen species (ROS). Melatonin (MT) has antioxidant proprieties and protects mitochondrial function. In this study, we evaluated ... ...

Abstract	Type II pneumocytes are the target of the SARS-CoV-2 virus, which alters their redox homeostasis to increase reactive oxygen species (ROS). Melatonin (MT) has antioxidant proprieties and protects mitochondrial function. In this study, we evaluated whether treatment with MT compensated for the redox homeostasis alteration in serum from COVID-19 patients. We determined oxidative stress (OS) markers such as carbonyls, glutathione (GSH), total antioxidant capacity (TAC), thiols, nitrites (NO
MeSH term(s)	Melatonin/therapeutic use ; Melatonin/pharmacology ; Humans ; Oxidation-Reduction/drug effects ; COVID-19/metabolism ; COVID-19/virology ; COVID-19/blood ; Homeostasis/drug effects ; Antioxidants/metabolism ; Antioxidants/therapeutic use ; Oxidative Stress/drug effects ; Male ; Female ; COVID-19 Drug Treatment ; Middle Aged ; SARS-CoV-2/drug effects ; Lipid Peroxidation/drug effects ; Aged ; Adult ; Reactive Oxygen Species/metabolism ; Glutathione/metabolism ; Glutathione/blood
Chemical Substances	Melatonin (JL5DK93RCL) ; Antioxidants ; Reactive Oxygen Species ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2024-04-21
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/ijms25084543
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Article ; Online: The Possible Role of Glucose-6-Phosphate Dehydrogenase in the SARS-CoV-2 Infection.

Pérez-Torres, Israel / Soto, María Elena / Guarner-Lans, Verónica / Manzano-Pech, Linaloe / Soria-Castro, Elizabeth

Cells

2022 Volume 11, Issue 13

Abstract: Glucose-6-phosphate dehydrogenase (G6PD) is the second rate-limiting enzyme of the pentose phosphate pathway. This enzyme is present in the cytoplasm of all mammalian cells, and its activity is essential for an adequate functioning of the antioxidant ... ...

Abstract	Glucose-6-phosphate dehydrogenase (G6PD) is the second rate-limiting enzyme of the pentose phosphate pathway. This enzyme is present in the cytoplasm of all mammalian cells, and its activity is essential for an adequate functioning of the antioxidant system and for the response of innate immunity. It is responsible for the production of nicotinamide adenine dinucleotide phosphate (NADPH), the first redox equivalent, in the pentose phosphate pathway. Viral infections such as SARS-CoV-2 may induce the Warburg effect with an increase in anaerobic glycolysis and production of lactate. This condition ensures the success of viral replication and production of the virion. Therefore, the activity of G6PD may be increased in COVID-19 patients raising the level of the NADPH, which is needed for the enzymatic and non-enzymatic antioxidant systems that counteract the oxidative stress caused by the cytokine storm. G6PD deficiency affects approximately 350-400 million people worldwide; therefore, it is one of the most prevalent diseases related to enzymatic deficiency worldwide. In G6PD-deficient patients exposed to SARS-CoV-2, the amount of NADPH is reduced, increasing the susceptibility for viral infection. There is loss of the redox homeostasis in them, resulting in severe pneumonia and fatal outcomes.
MeSH term(s)	Animals ; Antioxidants ; COVID-19 ; Glucosephosphate Dehydrogenase/metabolism ; Humans ; Mammals/metabolism ; NADP/metabolism ; SARS-CoV-2
Chemical Substances	Antioxidants ; NADP (53-59-8) ; Glucosephosphate Dehydrogenase (EC 1.1.1.49)
Language	English
Publishing date	2022-06-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11131982
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Article ; Online: Sulforaphane modifies mitochondrial-endoplasmic reticulum associations through reductive stress in cardiomyocytes.

Silva-Palacios, Alejandro / Arana-Hidalgo, Dana / Colín-Val, Zaira / Castrejón-Téllez, Vicente / Soria-Castro, Elizabeth / Pedraza-Chaverrí, José / López-Marure, Rebeca / Zazueta, Cecilia

Chemico-biological interactions

2023 Volume 382, Page(s) 110616

Abstract: Mitochondria-endoplasmic reticulum (ER) communication relies on platforms formed at the ER membrane with the mitochondrial outer membrane contact sites (MERCs). MERCs are involved in several processes including the unfolded protein response (UPR) and ... ...

Abstract	Mitochondria-endoplasmic reticulum (ER) communication relies on platforms formed at the ER membrane with the mitochondrial outer membrane contact sites (MERCs). MERCs are involved in several processes including the unfolded protein response (UPR) and calcium (Ca
MeSH term(s)	Myocytes, Cardiac/metabolism ; Mitochondria ; Endoplasmic Reticulum ; Unfolded Protein Response ; Endoplasmic Reticulum Stress
Chemical Substances	sulforaphane (GA49J4310U)
Language	English
Publishing date	2023-06-28
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2023.110616
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Article ; Online: Actin-Cytoskeleton Drives Caveolae Signaling to Mitochondria during Postconditioning.

Correa, Francisco / Enríquez-Cortina, Cristina / Silva-Palacios, Alejandro / Román-Anguiano, Nadia / Gil-Hernández, Aurora / Ostolga-Chavarría, Marcos / Soria-Castro, Elizabeth / Hernández-Rizo, Sharik / de Los Heros, Paola / Chávez-Canales, María / Zazueta, Cecilia

Cells

2023 Volume 12, Issue 3

Abstract: Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning. In this work, we evaluated the role that the actin-cytoskeleton network ... ...

Abstract	Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning. In this work, we evaluated the role that the actin-cytoskeleton network exerts on caveolae-mitochondria communication during postconditioning. Isolated rat hearts subjected to I/R and to postconditioning were treated with latrunculin A, a cytoskeleton disruptor. Cardiac function was compared between these hearts and those exposed only to I/R and to the cardioprotective maneuver. Caveolae and mitochondria structures were determined by electron microscopy and maintenance of the actin-cytoskeleton was evaluated by phalloidin staining. Caveolin-3 and other putative caveolae-conforming proteins were detected by immunoblot analysis. Co-expression of caveolin-3 and actin was evaluated both in lipid raft fractions and in heart tissue from the different groups. Mitochondrial function was assessed by respirometry and correlated with cholesterol levels. Treatment with latrunculin A abolishes the cardioprotective postconditioning effect, inducing morphological and structural changes in cardiac tissue, reducing F-actin staining and diminishing caveolae formation. Latrunculin A administration to post-conditioned hearts decreases the interaction between caveolae-forming proteins, the co-localization of caveolin with actin and inhibits oxygen consumption rates in both subsarcolemmal and interfibrillar mitochondria. We conclude that actin-cytoskeleton drives caveolae signaling to mitochondria during postconditioning, supporting their functional integrity and contributing to cardiac adaption against reperfusion injury.
MeSH term(s)	Rats ; Animals ; Caveolae/metabolism ; Actins/metabolism ; Caveolin 3/metabolism ; Cytoskeleton/metabolism ; Caveolin 1/metabolism ; Reperfusion Injury/metabolism ; Mitochondria/metabolism
Chemical Substances	latrunculin A (SRQ9WWM084) ; Actins ; Caveolin 3 ; Caveolin 1
Language	English
Publishing date	2023-02-02
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/cells12030492
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Article ; Online: PPAR Alpha Activation by Clofibrate Alleviates Ischemia/Reperfusion Injury in Metabolic Syndrome Rats by Decreasing Cardiac Inflammation and Remodeling and by Regulating the Atrial Natriuretic Peptide Compensatory Response.

Sánchez-Aguilar, María / Ibarra-Lara, Luz / Cano-Martínez, Agustina / Soria-Castro, Elizabeth / Castrejón-Téllez, Vicente / Pavón, Natalia / Osorio-Yáñez, Citlalli / Díaz-Díaz, Eulises / Rubio-Ruíz, María Esther

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Metabolic syndrome (MetS) is a cluster of factors that increase the risk of developing diabetes, stroke, and heart failure. The pathophysiology of injury by ischemia/reperfusion (I/R) is highly complex and the inflammatory condition plays an important ... ...

Abstract	Metabolic syndrome (MetS) is a cluster of factors that increase the risk of developing diabetes, stroke, and heart failure. The pathophysiology of injury by ischemia/reperfusion (I/R) is highly complex and the inflammatory condition plays an important role by increasing matrix remodeling and cardiac apoptosis. Natriuretic peptides (NPs) are cardiac hormones with numerous beneficial effects mainly mediated by a cell surface receptor named atrial natriuretic peptide receptor (ANPr). Although NPs are powerful clinical markers of cardiac failure, their role in I/R is still controversial. Peroxisome proliferator-activated receptor α agonists exert cardiovascular therapeutic actions; however, their effect on the NPs' signaling pathway has not been extensively studied. Our study provides important insight into the regulation of both ANP and ANPr in the hearts of MetS rats and their association with the inflammatory conditions caused by damage from I/R. Moreover, we show that pre-treatment with clofibrate was able to decrease the inflammatory response that, in turn, decreases myocardial fibrosis, the expression of metalloprotease 2 and apoptosis. Treatment with clofibrate is also associated with a decrease in ANP and ANPr expression.
MeSH term(s)	Rats ; Animals ; Atrial Natriuretic Factor/metabolism ; PPAR alpha/agonists ; Clofibrate/pharmacology ; Metabolic Syndrome/complications ; Metabolic Syndrome/drug therapy ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Receptors, Atrial Natriuretic Factor/metabolism ; Natriuretic Peptides ; Ischemia ; Arrhythmias, Cardiac ; Inflammation/drug therapy
Chemical Substances	Atrial Natriuretic Factor (85637-73-6) ; PPAR alpha ; Clofibrate (HPN91K7FU3) ; Receptors, Atrial Natriuretic Factor (EC 4.6.1.2) ; Natriuretic Peptides
Language	English
Publishing date	2023-03-10
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/ijms24065321
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Article ; Online: Reduced Levels of Selenium and Thioredoxin Reductase in the Thoracic Aorta Could Contribute to Aneurysm Formation in Patients with Marfan Syndrome.

Soto, María Elena / Pérez-Torres, Israel / Manzano-Pech, Linaloe / Soria-Castro, Elizabeth / Morales-Marín, Almilcar / Ramírez-Marroquín, Edgar Samuel / Martínez-Hernández, Humberto / Herrera-Alarcón, Valentín / Guarner-Lans, Verónica

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Marfan syndrome (MFS) is an autosomal dominant disorder caused by a heterozygous mutation of the FBN1 gene. MFS patients present oxidative stress that disturbs redox homeostasis. Redox homeostasis depends in part on the enzymatic antioxidant system, ... ...

Abstract	Marfan syndrome (MFS) is an autosomal dominant disorder caused by a heterozygous mutation of the FBN1 gene. MFS patients present oxidative stress that disturbs redox homeostasis. Redox homeostasis depends in part on the enzymatic antioxidant system, which includes thioredoxin reductase (TrxR) and glutathione peroxidases (GPx), both of which require an adequate concentration of selenium (Se). Therefore, the aim of this study was to determine if Se levels are decreased in the TAA of patients with MFS since this could contribute to the formation of an aneurysm in these patients. The results show that interleukins IL-1β, IL-6 TGF-β1, and TNF-α (
MeSH term(s)	Humans ; Selenium ; Aorta, Thoracic ; Thioredoxin-Disulfide Reductase ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Marfan Syndrome ; Aneurysm/complications ; Glutathione Peroxidase
Chemical Substances	Selenium (H6241UJ22B) ; Thioredoxin-Disulfide Reductase (EC 1.8.1.9) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Glutathione Peroxidase (EC 1.11.1.9)
Language	English
Publishing date	2023-06-21
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/ijms241310429
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Article ; Online: The Possible Role of Glucose-6-Phosphate Dehydrogenase in the SARS-CoV-2 Infection

Israel Pérez-Torres / María Elena Soto / Verónica Guarner-Lans / Linaloe Manzano-Pech / Elizabeth Soria-Castro

Cells, Vol 11, Iss 1982, p

2022 Volume 1982

Abstract	Glucose-6-phosphate dehydrogenase (G6PD) is the second rate-limiting enzyme of the pentose phosphate pathway. This enzyme is present in the cytoplasm of all mammalian cells, and its activity is essential for an adequate functioning of the antioxidant system and for the response of innate immunity. It is responsible for the production of nicotinamide adenine dinucleotide phosphate (NADPH), the first redox equivalent, in the pentose phosphate pathway. Viral infections such as SARS-CoV-2 may induce the Warburg effect with an increase in anaerobic glycolysis and production of lactate. This condition ensures the success of viral replication and production of the virion. Therefore, the activity of G6PD may be increased in COVID-19 patients raising the level of the NADPH, which is needed for the enzymatic and non-enzymatic antioxidant systems that counteract the oxidative stress caused by the cytokine storm. G6PD deficiency affects approximately 350–400 million people worldwide; therefore, it is one of the most prevalent diseases related to enzymatic deficiency worldwide. In G6PD-deficient patients exposed to SARS-CoV-2, the amount of NADPH is reduced, increasing the susceptibility for viral infection. There is loss of the redox homeostasis in them, resulting in severe pneumonia and fatal outcomes.
Keywords	Glucose-6-phosphate dehydrogenase ; SARS-CoV-2 ; COVID-19 ; redox homeostasis ; Warburg effect ; pentose phosphate pathway ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Down Regulation of

Forero-Forero, Angela / López-Ramírez, Stephany / Felix, Ricardo / Hernández-Sánchez, Javier / Tesoro-Cruz, Emiliano / Orozco-Suárez, Sandra / Murbartián, Janet / Soria-Castro, Elizabeth / Olivares, Aleida / Bekker-Méndez, Carolina / Paredes-Cervantes, Vladimir / Oviedo, Norma

International journal of molecular sciences

2022 Volume 23, Issue 15

Abstract: The CatSper channel localizes exclusively in the flagella of sperm cells. The Catsper1 protein, together with three pore units, is essential for the CatSper Channel formation, which produces flagellum hyperactivation and confers sperm fertility. ...

Abstract	The CatSper channel localizes exclusively in the flagella of sperm cells. The Catsper1 protein, together with three pore units, is essential for the CatSper Channel formation, which produces flagellum hyperactivation and confers sperm fertility.
MeSH term(s)	Animals ; Calcium Channels/metabolism ; Calmodulin/genetics ; Calmodulin/metabolism ; Down-Regulation ; Fertility ; Imidazoles ; Male ; Mice ; SOX Transcription Factors/genetics ; Semen/metabolism ; Sperm Motility/physiology ; Spermatozoa/metabolism
Chemical Substances	Calcium Channels ; Calmodulin ; Catsper1 protein, mouse ; Imidazoles ; SOX Transcription Factors ; calmidazolium (4R9H38JAWL)
Language	English
Publishing date	2022-07-22
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/ijms23158070
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Article: Citicoline Modifies the Expression of Specific miRNAs Related to Cardioprotection in Patients with ST-Segment Elevation Myocardial Infarction Subjected to Coronary Angioplasty.

Silva-Palacios, Alejandro / Arroyo-Campuzano, Miguel / Flores-García, Mirthala / Patlán, Mariana / Hernández-Díazcouder, Adrián / Alcántara, Diego / Ramírez-Camacho, Ixchel / Arana-Hidalgo, Dana / Soria-Castro, Elizabeth / Sánchez, Fausto / González-Pacheco, Héctor / Zazueta, Cecilia

Pharmaceuticals (Basel, Switzerland)

2022 Volume 15, Issue 8

Abstract: Extracellular vesicles are recognized as signaling mediators between cells both in physiological and pathological communication. In this work, we explored the potential effect of citicoline to modify relevant proteins or miRNAs for cardioprotection in ... ...

Abstract	Extracellular vesicles are recognized as signaling mediators between cells both in physiological and pathological communication. In this work, we explored the potential effect of citicoline to modify relevant proteins or miRNAs for cardioprotection in the smallest population of such microvesicles; i.e., in exosomes from patients diagnosed with ST-segment elevation myocardial infarction (STEMI) undergoing coronary angioplasty. The plasma-exosome-enriched fraction from these patients was characterized. Their cellular origin was assessed by flow cytometry and Western blot, whereas miRNA expression was evaluated by real-time polymerase chain reaction (qRT-PCR). The content of caveolin-1, caveolin-3, and hnRNPA2B1, which play a relevant role in selective transport of miRNAs into microvesicles, along with the effect on cell viability of the exosomes obtained from citicoline-treated and untreated groups were also analyzed. Our results showed that hypoxic stress increases exosome release into the circulation. Moreover, we found that CD146+ increased in exosomes from citicoline-treated patients, while CD142+ decreased in these patients compared to the placebo group. No changes were detected in the protein levels of caveolin-1, caveolin-3, and hnRNPA2B1. Citicoline administration modified the expression of miR233-3p, miR92, and miR21-5p in exosomes. Cell viability decreased in the presence of exosomes from infarcted patients, while incubation of H9c2 cells with exosomes from patients reperfused with citicoline did not affect cell viability. In conclusion, citicoline administration modifies the expression of specific miRNAs related to cardioprotection in exosomes.
Language	English
Publishing date	2022-07-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph15080925
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