LIVIVO - Search results -

Search results

Result 1 - 7 of total 7

Search options

Article: HDL Composition, Heart Failure, and Its Comorbidities.

Diab, Ahmed / Valenzuela Ripoll, Carla / Guo, Zhen / Javaheri, Ali

2022 Volume 9, Page(s) 846990

Abstract: Although research on high-density lipoprotein (HDL) has historically focused on atherosclerotic coronary disease, there exists untapped potential of HDL biology for the treatment of heart failure. Anti-oxidant, anti-inflammatory, and endothelial ... ...

Abstract	Although research on high-density lipoprotein (HDL) has historically focused on atherosclerotic coronary disease, there exists untapped potential of HDL biology for the treatment of heart failure. Anti-oxidant, anti-inflammatory, and endothelial protective properties of HDL could impact heart failure pathogenesis. HDL-associated proteins such as apolipoprotein A-I and M may have significant therapeutic effects on the myocardium, in part by modulating signal transduction pathways and sphingosine-1-phosphate biology. Furthermore, because heart failure is a complex syndrome characterized by multiple comorbidities, there are complex interactions between heart failure, its comorbidities, and lipoprotein homeostatic mechanisms. In this review, we will discuss the effects of heart failure and associated comorbidities on HDL, explore potential cardioprotective properties of HDL, and review novel HDL therapeutic targets in heart failure.
Language	English
Publishing date	2022-03-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.846990
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: JMJD6 protects against isoproterenol-induced cardiac hypertrophy via inhibition of NF-κB activation by demethylating R149 of the p65 subunit.

Guo, Zhen / Hu, Yue-Huai / Feng, Guo-Shuai / Valenzuela Ripoll, Carla / Li, Zhen-Zhen / Cai, Si-Dong / Wang, Qian-Qian / Luo, Wen-Wei / Li, Qian / Liang, Li-Ying / Wu, Zhong-Kai / Zhang, Ji-Guo / Javaheri, Ali / Wang, Lei / Lu, Jing / Liu, Pei-Qing

Acta pharmacologica Sinica

2023 Volume 44, Issue 9, Page(s) 1777–1789

Abstract: Histone modification plays an important role in pathological cardiac hypertrophy and heart failure. In this study we investigated the role of a histone arginine demethylase, Jumonji C domain-containing protein 6 (JMJD6) in pathological cardiac ... ...

Abstract	Histone modification plays an important role in pathological cardiac hypertrophy and heart failure. In this study we investigated the role of a histone arginine demethylase, Jumonji C domain-containing protein 6 (JMJD6) in pathological cardiac hypertrophy. Cardiac hypertrophy was induced in rats by subcutaneous injection of isoproterenol (ISO, 1.2 mg·kg
MeSH term(s)	Animals ; Rats ; Cardiomegaly/chemically induced ; Cardiomegaly/prevention & control ; Cardiomegaly/drug therapy ; Heart Failure/metabolism ; Histones/metabolism ; Isoproterenol/toxicity ; Myocytes, Cardiac/metabolism ; NF-kappa B/metabolism ; Rats, Sprague-Dawley ; RNA, Guide, CRISPR-Cas Systems ; Stroke Volume
Chemical Substances	Histones ; Isoproterenol (L628TT009W) ; NF-kappa B ; RNA, Guide, CRISPR-Cas Systems ; Jmjd6 protein, rat (EC 1.14.11.-)
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1360774-1
ISSN	1745-7254 ; 0253-9756 ; 1671-4083
ISSN (online)	1745-7254
ISSN	0253-9756 ; 1671-4083
DOI	10.1038/s41401-023-01086-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1904: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy.

Dhingra, Rimpy / Rabinovich-Nikitin, Inna / Rothman, Sonny / Guberman, Matthew / Gang, Hongying / Margulets, Victoria / Jassal, Davinder S / Alagarsamy, Keshav Narayan / Dhingra, Sanjiv / Valenzuela Ripoll, Carla / Billia, Filio / Diwan, Abhinav / Javaheri, Ali / Kirshenbaum, Lorrie A

Circulation

2022 Volume 146, Issue 12, Page(s) 934–954

Abstract: Background: Cytokines such as tumor necrosis factor-α (TNFα) have been implicated in cardiac dysfunction and toxicity associated with doxorubicin (DOX). Although TNFα can elicit different cellular responses, including survival or death, the mechanisms ... ...

Abstract	Background: Cytokines such as tumor necrosis factor-α (TNFα) have been implicated in cardiac dysfunction and toxicity associated with doxorubicin (DOX). Although TNFα can elicit different cellular responses, including survival or death, the mechanisms underlying these divergent outcomes in the heart remain cryptic. The E3 ubiquitin ligase TRAF2 (TNF receptor associated factor 2) provides a critical signaling platform for K63-linked polyubiquitination of RIPK1 (receptor interacting protein 1), crucial for nuclear factor-κB (NF-κB) activation by TNFα and survival. Here, we investigate alterations in TNFα-TRAF2-NF-κB signaling in the pathogenesis of DOX cardiotoxicity. Methods: Using a combination of in vivo (4 weekly injections of DOX 5 mg·kg Results: In contrast to vehicle-treated mice, ultrastructural defects, including cytoplasmic swelling, mitochondrial perturbations, and elevated TNFα levels, were observed in the hearts of mice treated with DOX. While investigating the involvement of TNFα in DOX cardiotoxicity, we discovered that NF-κB was readily activated by TNFα. However, TNFα-mediated NF-κB activation was impaired in cardiac myocytes treated with DOX. This coincided with loss of K63- linked polyubiquitination of RIPK1 from the proteasomal degradation of TRAF2. Furthermore, TRAF2 protein abundance was markedly reduced in hearts of patients with cancer treated with DOX. We further established that the reciprocal actions of the ubiquitinating and deubiquitinating enzymes cellular inhibitors of apoptosis 1 and USP19 (ubiquitin-specific peptidase 19), respectively, regulated the proteasomal degradation of TRAF2 in DOX-treated cardiac myocytes. An E3-ligase mutant of cellular inhibitors of apoptosis 1 (H588A) or gain of function of USP19 prevented proteasomal degradation of TRAF2 and DOX-induced cell death. Furthermore, wild-type TRAF2, but not a RING finger mutant defective for K63-linked polyubiquitination of RIPK1, restored NF-κB signaling and suppressed DOX-induced cardiac cell death. Last, cardiomyocyte-restricted expression of TRAF2 (cardiac troponin T-adeno-associated virus 9-TRAF2) in vivo protected against mitochondrial defects and cardiac dysfunction induced by DOX. Conclusions: Our findings reveal a novel signaling axis that functionally connects the cardiotoxic effects of DOX to proteasomal degradation of TRAF2. Disruption of the critical TRAF2 survival pathway by DOX sensitizes cardiac myocytes to TNFα-mediated necrotic cell death and DOX cardiotoxicity.
MeSH term(s)	Animals ; Apoptosis ; Cardiomyopathies/metabolism ; Cardiotoxicity ; Deubiquitinating Enzymes/metabolism ; Doxorubicin/toxicity ; Endopeptidases ; Humans ; Lactate Dehydrogenases/metabolism ; Mice ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; NF-kappa B/metabolism ; Rats ; TNF Receptor-Associated Factor 2/genetics ; Troponin T/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin-Specific Proteases/metabolism ; Ubiquitin-Specific Proteases/pharmacology
Chemical Substances	NF-kappa B ; PSMD2 protein, human ; TNF Receptor-Associated Factor 2 ; Troponin T ; Tumor Necrosis Factor-alpha ; Doxorubicin (80168379AG) ; Lactate Dehydrogenases (EC 1.1.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Endopeptidases (EC 3.4.-) ; USP19 protein, human (EC 3.4.-) ; Deubiquitinating Enzymes (EC 3.4.19.12) ; Ubiquitin-Specific Proteases (EC 3.4.19.12)
Language	English
Publishing date	2022-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.121.058411
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.60: 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: Sustained alternate-day fasting potentiates doxorubicin cardiotoxicity.

Cell metabolism

2023 Volume 35, Issue 6, Page(s) 928–942.e4

Abstract: Fasting strategies are under active clinical investigation in patients receiving chemotherapy. Prior murine studies suggest that alternate-day fasting may attenuate doxorubicin cardiotoxicity and stimulate nuclear translocation of transcription factor EB ...

Abstract	Fasting strategies are under active clinical investigation in patients receiving chemotherapy. Prior murine studies suggest that alternate-day fasting may attenuate doxorubicin cardiotoxicity and stimulate nuclear translocation of transcription factor EB (TFEB), a master regulator of autophagy and lysosomal biogenesis. In this study, human heart tissue from patients with doxorubicin-induced heart failure demonstrated increased nuclear TFEB protein. In mice treated with doxorubicin, alternate-day fasting or viral TFEB transduction increased mortality and impaired cardiac function. Mice randomized to alternate-day fasting plus doxorubicin exhibited increased TFEB nuclear translocation in the myocardium. When combined with doxorubicin, cardiomyocyte-specific TFEB overexpression provoked cardiac remodeling, while systemic TFEB overexpression increased growth differentiation factor 15 (GDF15) and caused heart failure and death. Cardiomyocyte TFEB knockout attenuated doxorubicin cardiotoxicity, while recombinant GDF15 was sufficient to cause cardiac atrophy. Our studies identify that both sustained alternate-day fasting and a TFEB/GDF15 pathway exacerbate doxorubicin cardiotoxicity.
MeSH term(s)	Mice ; Humans ; Animals ; Cardiotoxicity/metabolism ; Doxorubicin/toxicity ; Autophagy ; Myocytes, Cardiac/metabolism ; Fasting ; Heart Failure/chemically induced ; Heart Failure/metabolism ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Lysosomes/metabolism
Chemical Substances	Doxorubicin (80168379AG) ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.02.006
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6169: 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: Heterogeneous cardiac sympathetic innervation gradients promote arrhythmogenesis in murine dilated cardiomyopathy.

Dajani, Al-Hassan J / Liu, Michael B / Olaopa, Michael A / Cao, Lucian / Valenzuela-Ripoll, Carla / Davis, Timothy J / Poston, Megan D / Smith, Elizabeth H / Contreras, Jaime / Pennino, Marissa / Waldmann, Christopher M / Hoover, Donald B / Lee, Jason T / Jay, Patrick Y / Javaheri, Ali / Slavik, Roger / Qu, Zhilin / Ajijola, Olujimi A

JCI insight

2023 Volume 8, Issue 22

Abstract: Ventricular arrhythmias (VAs) in heart failure are enhanced by sympathoexcitation. However, radiotracer studies of catecholamine uptake in failing human hearts demonstrate a proclivity for VAs in patients with reduced cardiac sympathetic innervation. We ... ...

Abstract	Ventricular arrhythmias (VAs) in heart failure are enhanced by sympathoexcitation. However, radiotracer studies of catecholamine uptake in failing human hearts demonstrate a proclivity for VAs in patients with reduced cardiac sympathetic innervation. We hypothesized that this counterintuitive finding is explained by heterogeneous loss of sympathetic nerves in the failing heart. In a murine model of dilated cardiomyopathy (DCM), delayed PET imaging of sympathetic nerve density using the catecholamine analog [11C]meta-Hydroxyephedrine demonstrated global hypoinnervation in ventricular myocardium. Although reduced, sympathetic innervation in 2 distinct DCM models invariably exhibited transmural (epicardial to endocardial) gradients, with the endocardium being devoid of sympathetic nerve fibers versus controls. Further, the severity of transmural innervation gradients was correlated with VAs. Transmural innervation gradients were also identified in human left ventricular free wall samples from DCM versus controls. We investigated mechanisms underlying this relationship by in silico studies in 1D, 2D, and 3D models of failing and normal human hearts, finding that arrhythmogenesis increased as heterogeneity in sympathetic innervation worsened. Specifically, both DCM-induced myocyte electrical remodeling and spatially inhomogeneous innervation gradients synergistically worsened arrhythmogenesis. Thus, heterogeneous innervation gradients in DCM promoted arrhythmogenesis. Restoration of homogeneous sympathetic innervation in the failing heart may reduce VAs.
MeSH term(s)	Humans ; Mice ; Animals ; Cardiomyopathy, Dilated/diagnostic imaging ; Heart ; Myocardium ; Arrhythmias, Cardiac/diagnostic imaging ; Catecholamines
Chemical Substances	Catecholamines
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.157956
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: Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.

Guo, Zhen / Valenzuela Ripoll, Carla / Picataggi, Antonino / Rawnsley, David R / Ozcan, Mualla / Chirinos, Julio A / Chendamarai, Ezhilarasi / Girardi, Amanda / Riehl, Terrence / Evie, Hosannah / Diab, Ahmed / Kovacs, Attila / Hyrc, Krzysztof / Ma, Xiucui / Asnani, Aarti / Shewale, Swapnil V / Scherrer-Crosbie, Marielle / Cowart, Lauren Ashley / Parks, John S /

Zhao, Lei / Gordon, David / Ramirez-Valle, Francisco / Margulies, Kenneth B / Cappola, Thomas P / Desai, Ankit A / Pedersen, Lauren N / Bergom, Carmen / Stitziel, Nathan O / Rettig, Michael P / DiPersio, John F / Hajny, Stefan / Christoffersen, Christina / Diwan, Abhinav / Javaheri, Ali

JACC. Basic to translational science

2023 Volume 8, Issue 3, Page(s) 340–355

Abstract: Apolipoprotein M (ApoM) binds sphingosine-1-phosphate (S1P) and is inversely associated with mortality in human heart failure (HF). Here, we show that anthracyclines such as doxorubicin (Dox) reduce circulating ApoM in mice and humans, that ApoM is ... ...

Abstract	Apolipoprotein M (ApoM) binds sphingosine-1-phosphate (S1P) and is inversely associated with mortality in human heart failure (HF). Here, we show that anthracyclines such as doxorubicin (Dox) reduce circulating ApoM in mice and humans, that ApoM is inversely associated with mortality in patients with anthracycline-induced heart failure, and ApoM heterozygosity in mice increases Dox-induced mortality. In the setting of Dox stress, our studies suggest ApoM can help sustain myocardial autophagic flux in a post-transcriptional manner, attenuate Dox cardiotoxicity, and prevent lysosomal injury.
Language	English
Publishing date	2023-01-04
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2022.09.010
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: Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.

Pedersen, Lauren N / Valenzuela Ripoll, Carla / Ozcan, Mualla / Guo, Zhen / Lotfinaghsh, Aynaz / Zhang, Shiyang / Ng, Sherwin / Weinheimer, Carla / Nigro, Jessica / Kovacs, Attila / Diab, Ahmed / Klaas, Amanda / Grogan, Felicia / Cho, Yoonje / Ataran, Anahita / Luehmann, Hannah / Heck, Abigail / Kolb, Kollin / Strong, Lori /

Navara, Rachita / Walls, Gerard M / Hugo, Geoff / Samson, Pamela / Cooper, Daniel / Reynoso, Francisco J / Schwarz, Julie K / Moore, Kaitlin / Lavine, Kory / Rentschler, Stacey L / Liu, Yongjian / Woodard, Pamela K / Robinson, Clifford / Cuculich, Phillip S / Bergom, Carmen / Javaheri, Ali

Med (New York, N.Y.)

2023 Volume 4, Issue 12, Page(s) 928–943.e5

Abstract: Background: Rapidly dividing cells are more sensitive to radiation therapy (RT) than quiescent cells. In the failing myocardium, macrophages and fibroblasts mediate collateral tissue injury, leading to progressive myocardial remodeling, fibrosis, and ... ...

Abstract	Background: Rapidly dividing cells are more sensitive to radiation therapy (RT) than quiescent cells. In the failing myocardium, macrophages and fibroblasts mediate collateral tissue injury, leading to progressive myocardial remodeling, fibrosis, and pump failure. Because these cells divide more rapidly than cardiomyocytes, we hypothesized that macrophages and fibroblasts would be more susceptible to lower doses of radiation and that cardiac radiation could therefore attenuate myocardial remodeling. Methods: In three independent murine heart failure models, including models of metabolic stress, ischemia, and pressure overload, mice underwent 5 Gy cardiac radiation or sham treatment followed by echocardiography. Immunofluorescence, flow cytometry, and non-invasive PET imaging were employed to evaluate cardiac macrophages and fibroblasts. Serial cardiac magnetic resonance imaging (cMRI) from patients with cardiomyopathy treated with 25 Gy cardiac RT for ventricular tachycardia (VT) was evaluated to determine changes in cardiac function. Findings: In murine heart failure models, cardiac radiation significantly increased LV ejection fraction and reduced end-diastolic volume vs. sham. Radiation resulted in reduced mRNA abundance of B-type natriuretic peptide and fibrotic genes, and histological assessment of the LV showed reduced fibrosis. PET and flow cytometry demonstrated reductions in pro-inflammatory macrophages, and immunofluorescence demonstrated reduced proliferation of macrophages and fibroblasts with RT. In patients who were treated with RT for VT, cMRI demonstrated decreases in LV end-diastolic volume and improvements in LV ejection fraction early after treatment. Conclusions: These results suggest that 5 Gy cardiac radiation attenuates cardiac remodeling in mice and humans with heart failure. Funding: NIH, ASTRO, AHA, Longer Life Foundation.
MeSH term(s)	Humans ; Mice ; Animals ; Ventricular Remodeling ; Cardiomyopathies/complications ; Heart Failure/radiotherapy ; Heart Failure/drug therapy ; Heart Failure/etiology ; Myocytes, Cardiac/metabolism ; Ventricular Function ; Fibrosis
Language	English
Publishing date	2023-11-28
Publishing country	United States
Document type	Journal Article
ISSN	2666-6340
ISSN (online)	2666-6340
DOI	10.1016/j.medj.2023.10.006
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.

To top

Search results

Search options

Article: HDL Composition, Heart Failure, and Its Comorbidities.

More links

Kategorien

Order via subito

Article ; Online: JMJD6 protects against isoproterenol-induced cardiac hypertrophy via inhibition of NF-κB activation by demethylating R149 of the p65 subunit.

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Article ; Online: Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy.

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Article ; Online: Sustained alternate-day fasting potentiates doxorubicin cardiotoxicity.

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Article ; Online: Heterogeneous cardiac sympathetic innervation gradients promote arrhythmogenesis in murine dilated cardiomyopathy.

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Article ; Online: Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Article ; Online: Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.

More links

Kategorien

Order via subito

Inter-library loan at ZB MED