LIVIVO - Search results -

Search results

Result 1 - 10 of total 88

Search options

Article ; Online: News From the Heart Natriuretic System.

Armando, Ines

2017 Volume 10, Issue 6

MeSH term(s)	Atrial Natriuretic Factor ; Blood Pressure ; Genome-Wide Association Study ; Humans ; Hypertension ; Natriuretic Peptide, Brain
Chemical Substances	Natriuretic Peptide, Brain (114471-18-0) ; Atrial Natriuretic Factor (85637-73-6)
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2477394-3
ISSN	1942-3268 ; 1942-325X
ISSN (online)	1942-3268
ISSN	1942-325X
DOI	10.1161/CIRCGENETICS.117.002011
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6731: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Dopamine Receptor D

Zeng, Chunyu / Armando, Ines / Yang, Jian / Jose, Pedro A

The Yale journal of biology and medicine

2023 Volume 96, Issue 1, Page(s) 95–105

Abstract: Essential hypertension is caused by the interaction of genetic, behavioral, and environmental factors. Abnormalities in the regulation of renal ion transport cause essential hypertension. The renal dopaminergic system, which inhibits sodium transport in ... ...

Abstract	Essential hypertension is caused by the interaction of genetic, behavioral, and environmental factors. Abnormalities in the regulation of renal ion transport cause essential hypertension. The renal dopaminergic system, which inhibits sodium transport in all the nephron segments, is responsible for at least 50% of renal sodium excretion under conditions of moderate sodium excess. Dopaminergic signals are transduced by two families of receptors that belong to the G protein-coupled receptor (GPCR) superfamily. D
MeSH term(s)	Humans ; Mice ; Animals ; Hypertension/genetics ; Kidney/metabolism ; Blood Pressure ; Dopamine/metabolism ; Essential Hypertension/genetics ; Essential Hypertension/complications ; Essential Hypertension/metabolism ; Sodium/metabolism ; G-Protein-Coupled Receptor Kinase 4/genetics ; G-Protein-Coupled Receptor Kinase 4/metabolism
Chemical Substances	Dopamine (VTD58H1Z2X) ; Sodium (9NEZ333N27) ; GRK4 protein, human (EC 2.7.11.16) ; G-Protein-Coupled Receptor Kinase 4 (EC 2.7.11.16)
Language	English
Publishing date	2023-03-31
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	200515-3
ISSN	1551-4056 ; 0044-0086
ISSN (online)	1551-4056
ISSN	0044-0086
DOI	10.59249/MKRR9549
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.197: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Anti-Inflammatory Effects of Peripheral Dopamine.

Moore, Shaun C / Vaz de Castro, Pedro A S / Yaqub, Daniel / Jose, Pedro A / Armando, Ines

International journal of molecular sciences

2023 Volume 24, Issue 18

Abstract: Dopamine is synthesized in the nervous system where it acts as a neurotransmitter. Dopamine is also synthesized in a number of peripheral organs as well as in several types of cells and has organ-specific functions and, as demonstrated more recently, is ... ...

Abstract	Dopamine is synthesized in the nervous system where it acts as a neurotransmitter. Dopamine is also synthesized in a number of peripheral organs as well as in several types of cells and has organ-specific functions and, as demonstrated more recently, is involved in the regulation of the immune response and inflammatory reaction. In particular, the renal dopaminergic system is very important in the regulation of sodium transport and blood pressure and is particularly sensitive to stimuli that cause oxidative stress and inflammation. This review is focused on how dopamine is synthesized in organs and tissues and the mechanisms by which dopamine and its receptors exert their effects on the inflammatory response.
MeSH term(s)	Humans ; Dopamine ; Blood Pressure ; Inflammation ; Ion Transport ; Radiopharmaceuticals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use
Chemical Substances	Dopamine (VTD58H1Z2X) ; Radiopharmaceuticals ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-09-07
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/ijms241813816
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Mitochondrial DNA-Mediated Inflammation in Acute Kidney Injury and Chronic Kidney Disease.

Jin, Lini / Yu, Binfeng / Armando, Ines / Han, Fei

Oxidative medicine and cellular longevity

2021 Volume 2021, Page(s) 9985603

Abstract: The integrity and function of mitochondria are essential for normal kidney physiology. Mitochondrial DNA (mtDNA) has been widely a concern in recent years because its abnormalities may result in disruption of aerobic respiration, cellular dysfunction, ... ...

Abstract	The integrity and function of mitochondria are essential for normal kidney physiology. Mitochondrial DNA (mtDNA) has been widely a concern in recent years because its abnormalities may result in disruption of aerobic respiration, cellular dysfunction, and even cell death. Particularly, aberrant mtDNA copy number (mtDNA-CN) is associated with the development of acute kidney injury and chronic kidney disease, and urinary mtDNA-CN shows the potential to be a promising indicator for clinical diagnosis and evaluation of kidney function. Several lines of evidence suggest that mtDNA may also trigger innate immunity, leading to kidney inflammation and fibrosis. In mechanism, mtDNA can be released into the cytoplasm under cell stress and recognized by multiple DNA-sensing mechanisms, including Toll-like receptor 9 (TLR9), cytosolic cGAS-stimulator of interferon genes (STING) signaling, and inflammasome activation, which then mediate downstream inflammatory cascades. In this review, we summarize the characteristics of these mtDNA-sensing pathways mediating inflammatory responses and their role in the pathogenesis of acute kidney injury, nondiabetic chronic kidney disease, and diabetic kidney disease. In addition, we highlight targeting of mtDNA-mediated inflammatory pathways as a novel therapeutic target for these kidney diseases.
MeSH term(s)	Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Animals ; DNA, Mitochondrial/metabolism ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Mitochondria/metabolism ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology
Chemical Substances	DNA, Mitochondrial ; Inflammation Mediators
Language	English
Publishing date	2021-06-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2021/9985603
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: ADAMs family in kidney physiology and pathology.

Zhu, Huanhuan / Wang, Junni / Nie, Wanyun / Armando, Ines / Han, Fei

EBioMedicine

2021 Volume 72, Page(s) 103628

Abstract: A disintegrin and metalloproteinases (ADAMs) family are proteolytic transmembrane proteases that modulate diverse cell functions and coordinate intercellular communication. ADAMs are responsible for regulating cell proliferation, differentiation, ... ...

Abstract	A disintegrin and metalloproteinases (ADAMs) family are proteolytic transmembrane proteases that modulate diverse cell functions and coordinate intercellular communication. ADAMs are responsible for regulating cell proliferation, differentiation, migration, and organ morphogenesis in kidney development. Abnormally activated ADAMs drive inflammation and fibrosis in response to kidney diseases such as acute kidney injury, diabetic kidney disease, polycystic kidney disease, and chronic allograft nephropathy. ADAM10 and ADAM17, known as the most characterized members of ADAMs, are extensively investigated in kidney diseases. Notably, ADAM proteases have the potential to be targets for developing novel treatment approaches in kidney diseases.
MeSH term(s)	ADAM Proteins/metabolism ; Animals ; Cell Communication/physiology ; Humans ; Inflammation/metabolism ; Kidney/metabolism ; Kidney Diseases/metabolism
Chemical Substances	ADAM Proteins (EC 3.4.24.-)
Language	English
Publishing date	2021-10-12
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2021.103628
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 7090: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: DOPAMINE D4 RECEPTOR DOWN-REGULATES RENAL SODIUM CHLORIDE COTRANSPORTER VIA UBIQUITINATION-ASSOCIATED LYSOSOME DEGRADATION.

Zhang, Mingzhuo / Liu, Mingda / Ren, Zhiyun / Wang, Weiwan / Upadhyay, Kiran / Asico, Laureano Asico / Armando, Ines / Jia, Yutao / Wang, Ping / Xue, Ying / Wang, Xiaoyan

bioRxiv : the preprint server for biology

2024

Abstract: Background: The thiazide-sensitive sodium chloride cotransporter (NCC) is the major apical sodium transporter located in the mammalian renal distal convoluted tubule (DCT). The amount of sodium reabsorbed in the DCT through NCC plays an important role ... ...

Abstract	Background: The thiazide-sensitive sodium chloride cotransporter (NCC) is the major apical sodium transporter located in the mammalian renal distal convoluted tubule (DCT). The amount of sodium reabsorbed in the DCT through NCC plays an important role in the regulation of extracellular fluid volume and blood pressure. Dopamine and its receptors constitute a renal antihypertensive system in mammals. The disruption of Drd4 in mice causes kidney-related hypertension. However, the pathogenesis of D4R-deficiency associated hypertension is not well documented. Method: We assessed the effects of D4R on NCC protein abundances and activities of DCT in mice with renal or global Drd4-deficiencies and expressing human D4.7 variant and in cultured mouse DCT cells, and explored the molecular mechanism. Results: NCC inhibitor hydrochlorothiazide enhanced the natriuresis in Drd4-/- mice. Renal NCC protein was greater while ubiquitination of NCC was less in Drd4-/- than Drd4+/+ mice. Silencing of D4R in cultured mouse DCT cells increased NCC protein but decreased NCC ubiquitination. D4R agonist had opposite effects that were blocked by the antagonist. In mouse kidneys and DCT cells D4R and NCC colocalized and co-immunoprecipitated. Moreover, D4R-agonist promoted the binding between the two proteins demonstrated by fluorescence resonance energy transfer. D4R agonism internalized NCC, decreased NCC in the plasma membrane, increased NCC in lysosomes and reduced NCC-dependent-intracellular-sodium transport. The lysosomal inhibitor chloroquine prevented the D4R-induced NCC-reduction. A shortened NCC half-life was suggested by its decay under cycloheximide-chase. Ubiquitin-specific-protease 48 (USP48, a deubiquitinating enzyme) was increased in the kidneys and cells with Drd4-deficiency while D4R stimulation decreased it in vitro and reduction of USP48 with siRNA decreased NCC expression. The mice carrying human D4.7 variant or with renal supcapsular-Drd4-siRNA-delivery developed hypertension with increased NCC. Conclusion: Our data demonstrates that D4R downregulates NCC by promoting USP48-associated deubiquitination and subsequent internalization, lysosome relocation and degradation.
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.14.580405
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: G Protein-Coupled Receptor 37L1 Modulates Epigenetic Changes in Human Renal Proximal Tubule Cells.

Armando, Ines / Cuevas, Santiago / Fan, Caini / Kumar, Megha / Izzi, Zahra / Jose, Pedro A / Konkalmatt, Prasad R

International journal of molecular sciences

2022 Volume 23, Issue 22

Abstract: Renal luminal sodium transport is essential for physiological blood pressure control, and abnormalities in this process are strongly implicated in the pathogenesis of essential hypertension. Renal G protein-coupled receptors (GPCRs) are critical for the ... ...

Abstract	Renal luminal sodium transport is essential for physiological blood pressure control, and abnormalities in this process are strongly implicated in the pathogenesis of essential hypertension. Renal G protein-coupled receptors (GPCRs) are critical for the regulation of the reabsorption of essential nutrients, ions, and water from the glomerular filtrate. Recently, we showed that GPCR 37L1 (GPR37L1) is expressed on the apical membrane of renal proximal tubules (RPT) and regulates luminal sodium transport and blood pressure by modulating the function of the sodium proton exchanger 3 (NHE3). However, little is known about GPR37L1 intracellular signaling. Here, we show that GPR37L1 is localized to the nuclear membrane, in addition to the plasma membrane in human RPT cells. Furthermore, GPR37L1 signals via the PI3K/AKT/mTOR pathway to decrease the expression of DNA (cytosine-5)-methyltransferase 1 (DNMT1) and enhance NHE3 transcription. Overall, we demonstrate the direct role of a nuclear membrane GPCR in the regulation of renal sodium through epigenetic gene regulation.
MeSH term(s)	Humans ; Sodium-Hydrogen Exchanger 3/genetics ; Sodium-Hydrogen Exchanger 3/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Sodium-Hydrogen Exchangers/genetics ; Sodium-Hydrogen Exchangers/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Sodium/metabolism ; Epigenesis, Genetic
Chemical Substances	Sodium-Hydrogen Exchanger 3 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Sodium-Hydrogen Exchangers ; Receptors, G-Protein-Coupled ; Sodium (9NEZ333N27) ; GPR37L1 protein, human
Language	English
Publishing date	2022-11-21
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/ijms232214456
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Inverse Salt Sensitivity of Blood Pressure: Mechanisms and Potential Relevance for Prevention of Cardiovascular Disease.

Felder, Robin A / Gildea, John J / Xu, Peng / Yue, Wei / Armando, Ines / Carey, Robert M / Jose, Pedro A

Current hypertension reports

2022 Volume 24, Issue 9, Page(s) 361–374

Abstract: Purpose of review: To review the etiology of inverse salt sensitivity of blood pressure (BP).: Recent findings: Both high and low sodium ( ... ...

Abstract	Purpose of review: To review the etiology of inverse salt sensitivity of blood pressure (BP). Recent findings: Both high and low sodium (Na
MeSH term(s)	Adult ; Blood Pressure/physiology ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/prevention & control ; Diet, Sodium-Restricted ; Humans ; Hypertension/drug therapy ; Hypertension/etiology ; Hypertension/prevention & control ; Sodium/therapeutic use ; Sodium Chloride ; Sodium Chloride, Dietary/adverse effects
Chemical Substances	Sodium Chloride, Dietary ; Sodium Chloride (451W47IQ8X) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2022-06-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2057367-4
ISSN	1534-3111 ; 1522-6417
ISSN (online)	1534-3111
ISSN	1522-6417
DOI	10.1007/s11906-022-01201-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5522: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Genomics and pharmacogenomics of salt-sensitive hypertension Minireview.

Armando, Ines / Villar, Van Anthony M / Jose, Pedro A

Current hypertension reviews

2017 Volume 11, Issue 1, Page(s) 49–56

Abstract: Salt sensitivity is estimated to be present in 51% of the hypertensive and 26% of the normotensive populations. The individual blood pressure response to salt is heterogeneous and possibly related to inherited susceptibility. Although the mechanisms ... ...

Abstract	Salt sensitivity is estimated to be present in 51% of the hypertensive and 26% of the normotensive populations. The individual blood pressure response to salt is heterogeneous and possibly related to inherited susceptibility. Although the mechanisms underlying salt sensitivity are complex and not well understood, genetics can help to determine the blood response to salt intake. So far only a few genes have been found to be associated with salt-sensitive hypertension using candidate gene association studies. The kidney is critical to overall fluid and electrolyte balance and long-term regulation of blood pressure. Thus, the pathogenesis of salt sensitivity must involve a derangement in renal NaCl handling: an inability to decrease renal sodium transport and increase sodium excretion in the face of an increase in NaCl load that could be caused by aberrant counter-regulatory natriuretic/antinatriuretic pathways. We review here the literature regarding the gene variants associated with salt-sensitive hypertension and how the presence of these gene variants influences the response to antihypertensive therapy.
Language	English
Publishing date	2017-04-06
Publishing country	United Arab Emirates
Document type	Journal Article
ISSN	1875-6506
ISSN (online)	1875-6506
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Peroxiredoxin-4 and Dopamine D5 Receptor Interact to Reduce Oxidative Stress and Inflammation in the Kidney.

Amatya, Bibhas / Yang, Sufei / Yu, Peiying / Vaz de Castro, Pedro A S / Armando, Ines / Zeng, Chunyu / Felder, Robin A / Asico, Laureano D / Jose, Pedro A / Lee, Hewang

Antioxidants & redox signaling

2023 Volume 38, Issue 16-18, Page(s) 1150–1166

Abstract: Aims: ...

Abstract	Aims:
MeSH term(s)	Mice ; Humans ; Animals ; Receptors, Dopamine D5/metabolism ; Interleukin-1beta/metabolism ; Hydrogen Peroxide/metabolism ; Caspase 12/metabolism ; HEK293 Cells ; Kidney/metabolism ; Fenoldopam/metabolism ; Fenoldopam/pharmacology ; Oxidative Stress ; Inflammation/metabolism ; Peroxiredoxins/genetics ; Peroxiredoxins/metabolism
Chemical Substances	Receptors, Dopamine D5 (137750-35-7) ; Interleukin-1beta ; Hydrogen Peroxide (BBX060AN9V) ; Caspase 12 (EC 3.4.22.-) ; Fenoldopam (INU8H2KAWG) ; Peroxiredoxins (EC 1.11.1.15) ; Drd5 protein, mouse
Language	English
Publishing date	2023-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2022.0034
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5488: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito