LIVIVO - Search results -

Search results

Result 1 - 10 of total 77

Search options

Article ; Online: The mitochondrial calcium uniporter in the heart: energetics and beyond.

Kwong, Jennifer Q

2017 Volume 595, Issue 12, Page(s) 3743–3751

Abstract: ... ...

Abstract	Ca
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Cell Death/physiology ; Excitation Contraction Coupling/physiology ; Humans ; Mitochondria, Heart/metabolism ; Mitochondrial Membranes/metabolism ; Myocytes, Cardiac/metabolism ; Ruthenium Red/metabolism
Chemical Substances	Calcium Channels ; mitochondrial calcium uniporter ; Ruthenium Red (11103-72-3) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-02-01
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP273059
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.65: 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: Mitochondrial functional resilience after TFAM ablation in the adult heart.

Ghazal, Nasab / Peoples, Jessica N / Mohiuddin, Tahmina A / Kwong, Jennifer Q

American journal of physiology. Cell physiology

2021 Volume 320, Issue 6, Page(s) C929–C942

Abstract: The nuclear genome-encoded mitochondrial DNA (mtDNA) transcription factor A (TFAM) is indispensable for mitochondrial energy production in the developing and postnatal heart; a similar role for TFAM is inferred in adult heart. Here, we provide evidence ... ...

Abstract	The nuclear genome-encoded mitochondrial DNA (mtDNA) transcription factor A (TFAM) is indispensable for mitochondrial energy production in the developing and postnatal heart; a similar role for TFAM is inferred in adult heart. Here, we provide evidence that challenges this long-standing paradigm. Unexpectedly, conditional
MeSH term(s)	Animals ; DNA Replication/genetics ; DNA, Mitochondrial/genetics ; DNA-Binding Proteins/genetics ; Down-Regulation/genetics ; Electron Transport/genetics ; Female ; Gene Expression Regulation/genetics ; Heart/physiology ; High Mobility Group Proteins/genetics ; Male ; Mice ; Mitochondria/genetics ; Mitochondrial Proteins/genetics ; Myocytes, Cardiac/metabolism ; Transcription Factors/genetics ; Transcription, Genetic/genetics
Chemical Substances	DNA, Mitochondrial ; DNA-Binding Proteins ; High Mobility Group Proteins ; Mitochondrial Proteins ; Tfam protein, mouse ; Transcription Factors
Language	English
Publishing date	2021-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00508.2020
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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: Sex differences in the involvement of skeletal and cardiac muscles in myopathic

Foltz, Steven / Wu, Fang / Ghazal, Nasab / Kwong, Jennifer Q / Hartzell, H Criss / Choo, Hyojung J

American journal of physiology. Cell physiology

2022 Volume 322, Issue 2, Page(s) C283–C295

Abstract: Limb-girdle muscular dystrophy R12 (LGMD-R12) is caused by recessive mutations in the Anoctamin-5 gene ( ...

Abstract	Limb-girdle muscular dystrophy R12 (LGMD-R12) is caused by recessive mutations in the Anoctamin-5 gene (
MeSH term(s)	Animals ; Anoctamins/deficiency ; Anoctamins/genetics ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cardiomyopathies/physiopathology ; Creatine Kinase/blood ; Exercise Tolerance ; Female ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Contraction ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscle, Skeletal/physiopathology ; Muscular Dystrophies, Limb-Girdle/genetics ; Muscular Dystrophies, Limb-Girdle/metabolism ; Muscular Dystrophies, Limb-Girdle/pathology ; Muscular Dystrophies, Limb-Girdle/physiopathology ; Myocardium/metabolism ; Myocardium/pathology ; Sex Characteristics ; Sex Factors ; Mice
Chemical Substances	ANO5 protein, human ; ANO5 protein, mouse ; Anoctamins ; Creatine Kinase (EC 2.7.3.2)
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00350.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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: Mitochondrial citrate carrier SLC25A1 is a dosage-dependent regulator of metabolic reprogramming and morphogenesis in the developing heart.

Ohanele, Chiemela / Peoples, Jessica N / Karlstaedt, Anja / Geiger, Joshua T / Gayle, Ashley D / Ghazal, Nasab / Sohani, Fateemaa / Brown, Milton E / Davis, Michael E / Porter, George A / Faundez, Victor / Kwong, Jennifer Q

bioRxiv : the preprint server for biology

2023

Abstract: The developing mammalian heart undergoes an important metabolic shift from glycolysis toward mitochondrial oxidation, such that oxidative phosphorylation defects may present with cardiac abnormalities. Here, we describe a new mechanistic link between ... ...

Abstract	The developing mammalian heart undergoes an important metabolic shift from glycolysis toward mitochondrial oxidation, such that oxidative phosphorylation defects may present with cardiac abnormalities. Here, we describe a new mechanistic link between mitochondria and cardiac morphogenesis, uncovered by studying mice with systemic loss of the mitochondrial citrate carrier SLC25A1.
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.22.541833
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: Physiological and pathological roles of the mitochondrial permeability transition pore in the heart.

Kwong, Jennifer Q / Molkentin, Jeffery D

Cell metabolism

2015 Volume 21, Issue 2, Page(s) 206–214

Abstract: Prolonged mitochondrial permeability transition pore (MPTP) opening results in mitochondrial energetic dysfunction, organelle swelling, rupture, and typically a type of necrotic cell death. However, acute opening of the MPTP has a critical physiologic ... ...

Abstract	Prolonged mitochondrial permeability transition pore (MPTP) opening results in mitochondrial energetic dysfunction, organelle swelling, rupture, and typically a type of necrotic cell death. However, acute opening of the MPTP has a critical physiologic role in regulating mitochondrial Ca(2+) handling and metabolism. Despite the physiological and pathological roles that the MPTP orchestrates, the proteins that comprise the pore itself remain an area of ongoing investigation. Here, we will discuss the molecular composition of the MPTP and its role in regulating cardiac physiology and disease. A better understanding of MPTP structure and function will likely suggest novel cardioprotective therapeutic approaches.
MeSH term(s)	Animals ; Calcium/metabolism ; Heart/physiology ; Humans ; Mitochondria, Heart/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Myocardium/metabolism ; Myocardium/pathology
Chemical Substances	Mitochondrial Membrane Transport Proteins ; mitochondrial permeability transition pore ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2014.12.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

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 ▾

Article ; Online: Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells.

Maxwell, Joshua T / Tsai, Chin-Hsien / Mohiuddin, Tahmina A / Kwong, Jennifer Q

Journal of visualized experiments : JoVE

2018 , Issue 134

Abstract: ... ...

Abstract	Ca
MeSH term(s)	Animals ; Calcium/metabolism ; Cells, Cultured ; Mice ; Microscopy, Confocal/methods ; Mitochondria/metabolism ; Mitochondria, Heart/metabolism ; Myocytes, Cardiac/metabolism
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/57225
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome.

Peoples, Jessica N / Ghazal, Nasab / Duong, Duc M / Hardin, Katherine R / Manning, Janet R / Seyfried, Nicholas T / Faundez, Victor / Kwong, Jennifer Q

American journal of physiology. Cell physiology

2021 Volume 321, Issue 3, Page(s) C519–C534

Abstract: Mitochondria are recognized as signaling organelles, because under stress, mitochondria can trigger various signaling pathways to coordinate the cell's response. The specific pathway(s) engaged by mitochondria in response to mitochondrial energy defects ... ...

Abstract	Mitochondria are recognized as signaling organelles, because under stress, mitochondria can trigger various signaling pathways to coordinate the cell's response. The specific pathway(s) engaged by mitochondria in response to mitochondrial energy defects in vivo and in high-energy tissues like the heart are not fully understood. Here, we investigated cardiac pathways activated in response to mitochondrial energy dysfunction by studying mice with cardiomyocyte-specific loss of the mitochondrial phosphate carrier (SLC25A3), an established model that develops cardiomyopathy as a result of defective mitochondrial ATP synthesis. Mitochondrial energy dysfunction induced a striking pattern of acylome remodeling, with significantly increased posttranslational acetylation and malonylation. Mass spectrometry-based proteomics further revealed that energy dysfunction-induced remodeling of the acetylome and malonylome preferentially impacts mitochondrial proteins. Acetylation and malonylation modified a highly interconnected interactome of mitochondrial proteins, and both modifications were present on the enzyme isocitrate dehydrogenase 2 (IDH2). Intriguingly, IDH2 activity was enhanced in SLC25A3-deleted mitochondria, and further study of IDH2 sites targeted by both acetylation and malonylation revealed that these modifications can have site-specific and distinct functional effects. Finally, we uncovered a novel cross talk between the two modifications, whereby mitochondrial energy dysfunction-induced acetylation of sirtuin 5 (SIRT5), inhibited its function. Because SIRT5 is a mitochondrial deacylase with demalonylase activity, this finding suggests that acetylation can modulate the malonylome. Together, our results position acylations as an arm of the mitochondrial response to energy dysfunction and suggest a mechanism by which focal disruption to the energy production machinery can have an expanded impact on global mitochondrial function.
MeSH term(s)	Acetylation ; Animals ; Biological Transport ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cation Transport Proteins/deficiency ; Cation Transport Proteins/genetics ; Energy Metabolism ; Female ; Gene Regulatory Networks ; Isocitrate Dehydrogenase/genetics ; Isocitrate Dehydrogenase/metabolism ; Male ; Malonates/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Heart/genetics ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/pathology ; Mitochondrial Proteins/deficiency ; Mitochondrial Proteins/genetics ; Models, Molecular ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Phosphate Transport Proteins/deficiency ; Phosphate Transport Proteins/genetics ; Phosphates ; Protein Conformation ; Protein Interaction Mapping ; Protein Processing, Post-Translational ; Signal Transduction ; Sirtuins/genetics ; Sirtuins/metabolism ; Solute Carrier Proteins/deficiency ; Solute Carrier Proteins/genetics
Chemical Substances	Cation Transport Proteins ; Malonates ; Mitochondrial Proteins ; Phosphate Transport Proteins ; Phosphates ; SIRT5 protein, mouse ; Slc25a3 protein, mouse ; Solute Carrier Proteins ; malonic acid (9KX7ZMG0MK) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; isocitrate dehydrogenase 2, mouse (EC 1.1.1.41) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00156.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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: Mitochondrial dysfunction and oxidative stress in heart disease.

Peoples, Jessica N / Saraf, Anita / Ghazal, Nasab / Pham, Tyler T / Kwong, Jennifer Q

Experimental & molecular medicine

2019 Volume 51, Issue 12, Page(s) 1–13

Abstract: Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated ... ...

Abstract	Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated process driving oxidative stress and disease pathology, contemporary studies reveal that ROS also facilitate normal physiology. Mitochondria are especially abundant in cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Moreover, there is growing appreciation that medical therapies designed to mediate mitochondrial ROS production can be important strategies to ameliorate cardiac disease. In this review, we highlight evidence from animal models that illustrates the strong connections between mitochondrial ROS and cardiac disease, discuss advancements in the development of mitochondria-targeted antioxidant therapies, and identify challenges faced in bringing such therapies into the clinic.
MeSH term(s)	Animals ; Cardiomyopathies/metabolism ; Heart Diseases/metabolism ; Humans ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2019-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-019-0355-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4775: 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

Article ; Online: Mitochondrial dysfunction and oxidative stress in heart disease

Jessica N. Peoples / Anita Saraf / Nasab Ghazal / Tyler T. Pham / Jennifer Q. Kwong

Experimental and Molecular Medicine, Vol 51, Iss 12, Pp 1-

2019 Volume 13

Abstract: ... by targeting signaling molecules that cause oxidative stress. Jennifer Kwong at Emory University School ...

Abstract	Heart disease: Signaling a halt to disease progression Heart disease progression could be tackled by targeting signaling molecules that cause oxidative stress. Jennifer Kwong at Emory University School of Medicine in Atlanta, USA, and co-workers reviewed research into the role of mitochondria and their associated signaling molecules in the development of heart disease. Mitochondria are a major source of reactive oxygen species (ROS), signaling molecules involved in muscle contraction and calcium transfer in the heart, but they also destroy ROS to maintain a balance. Disruption to this balance can lead to elevated ROS, causing DNA and cellular damage, triggering disease. Animal trials using drugs to target mitochondrial ROS show promise in limiting heart disease progression. Further research is needed to determine whether this approach will work in humans and which specific heart problems might benefit from such therapies.
Keywords	Medicine ; R ; Biochemistry ; QD415-436
Language	English
Publishing date	2019-12-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

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: Safety and Health Care Use Following COVID-19 Vaccination Among Adults With Rheumatoid Arthritis: A Population-Based Self-Controlled Case Series Analysis.

Lee, Jennifer J Y / Bernatsky, Sasha / Kwong, Jeffrey C / Li, Qing / Kwok, Timothy S H / Widdifield, Jessica

The Journal of rheumatology

2023

Abstract: Objective: To determine if coronavirus disease 2019 (COVID-19) vaccines were associated with adverse events of special interest (AESIs) and healthcare use among adults with rheumatoid arthritis (RA).: Methods: Among adults with RA who received at ... ...

Abstract	Objective: To determine if coronavirus disease 2019 (COVID-19) vaccines were associated with adverse events of special interest (AESIs) and healthcare use among adults with rheumatoid arthritis (RA). Methods: Among adults with RA who received at least 1 COVID-19 vaccine, a self-controlled case series (SCCS) analysis was conducted to evaluate relative incidence (RI) rates of AESIs (Bell palsy, idiopathic thrombocytopenia, acute disseminated encephalomyelitis, pericarditis/myocarditis, Guillain-Barré syndrome, transverse myelitis, myocardial infarction, anaphylaxis, stroke, deep vein thrombosis, pulmonary embolism, narcolepsy, appendicitis, and disseminated intravascular coagulation) in any 21-day period following vaccination compared to control periods. Secondary outcomes included emergency department (ED) visits, hospitalizations, and rheumatology visits. A matched non-RA comparator group was created and a separate SCCS analysis was conducted. RI ratios (RIRs) were used to compare RA and non-RA groups. Results: Among 123,466 patients with RA and 493,864 comparators, the majority received mRNA vaccines. For patients with RA, relative to control periods, AESIs were not increased. ED visits increased after dose 2 (RI 1.06, 95% CI 1.03-1.10) and decreased after dose 3 (RI 0.93, 95% CI 0.89-0.96). Hospitalizations were lower after the first (RI 0.83, 95% CI 0.78-0.88), second (RI 0.86, 95% CI 0.81-0.92), and third (RI 0.89, 95% CI 0.83-0.95) doses. Rheumatology visits increased after dose 1 (RI 1.08, 95% CI 1.07-1.10), and decreased after doses 2 and 3. Relative to comparators, patients with RA had a higher AESI risk after dose 3 (RIR 1.28, 95% CI 1.05-1.56). Patients with RA experienced fewer ED visits (RIR 0.73, 95% CI 0.58-0.90) and hospitalizations (RIR 0.52, 95% CI 0.36-0.75) after dose 4. Conclusion: COVID-19 vaccines in patients with RA were not associated with an increase in AESI risk or healthcare use after every dose.
Language	English
Publishing date	2023-10-01
Publishing country	Canada
Document type	Journal Article
ZDB-ID	194928-7
ISSN	1499-2752 ; 0315-162X
ISSN (online)	1499-2752
ISSN	0315-162X
DOI	10.3899/jrheum.2023-0355
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1168: 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)
Zs.MO 135: Show issues

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

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

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

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito