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Article ; Online: Placental Mitochondrial Function and Dysfunction in Preeclampsia.

Jahan, Fahmida / Vasam, Goutham / Green, Alex E / Bainbridge, Shannon A / Menzies, Keir J

International journal of molecular sciences

2023 Volume 24, Issue 4

Abstract: The placenta is a vital organ of pregnancy, regulating adaptation to pregnancy, gestational parent/fetal exchange, and ultimately, fetal development and growth. Not surprisingly, in cases of placental dysfunction-where aspects of placental development or ...

Abstract	The placenta is a vital organ of pregnancy, regulating adaptation to pregnancy, gestational parent/fetal exchange, and ultimately, fetal development and growth. Not surprisingly, in cases of placental dysfunction-where aspects of placental development or function become compromised-adverse pregnancy outcomes can result. One common placenta-mediated disorder of pregnancy is preeclampsia (PE), a hypertensive disorder of pregnancy with a highly heterogeneous clinical presentation. The wide array of clinical characteristics observed in pregnant individuals and neonates of a PE pregnancy are likely the result of distinct forms of placental pathology underlying the PE diagnosis, explaining why no one common intervention has proven effective in the prevention or treatment of PE. The historical paradigm of placental pathology in PE highlights an important role for utero-placental malperfusion, placental hypoxia and oxidative stress, and a critical role for placental mitochondrial dysfunction in the pathogenesis and progression of the disease. In the current review, the evidence of placental mitochondrial dysfunction in the context of PE will be summarized, highlighting how altered mitochondrial function may be a common feature across distinct PE subtypes. Further, advances in this field of study and therapeutic targeting of mitochondria as a promising intervention for PE will be discussed.
MeSH term(s)	Infant, Newborn ; Pregnancy ; Female ; Humans ; Pre-Eclampsia/pathology ; Placenta/pathology ; Pregnancy Outcome ; Hypertension/pathology ; Mitochondria/pathology ; Placenta Diseases/pathology
Language	English
Publishing date	2023-02-20
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/ijms24044177
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Article: A comparison of rat models that best mimic immune-driven preeclampsia in humans.

Jahan, Fahmida / Vasam, Goutham / Cariaco, Yusmaris / Nik-Akhtar, Abolfazl / Green, Alex / Menzies, Keir J / Bainbridge, Shannon A

Frontiers in endocrinology

2023 Volume 14, Page(s) 1219205

Abstract: Preeclampsia (PE), a hypertensive pregnancy disorder, can originate from varied etiology. Placenta malperfusion has long been considered the primary cause of PE. However, we and others have showed that this disorder can also result from heightened ... ...

Abstract	Preeclampsia (PE), a hypertensive pregnancy disorder, can originate from varied etiology. Placenta malperfusion has long been considered the primary cause of PE. However, we and others have showed that this disorder can also result from heightened inflammation at the maternal-fetal interface. To advance our understanding of this understudied PE subtype, it is important to establish validated rodent models to study the pathophysiology and test therapies. We evaluated three previously described approaches to induce inflammation-mediated PE-like features in pregnant rats: 1) Tumor necrosis factor-α (TNF-α) infusion via osmotic pump from gestational day (GD) 14-19 at 50ng/day/animal; 2) Polyinosinic:polycytidylic acid (Poly I:C) intraperitoneal (IP) injections from GD 10-18 (alternate days) at 10mg/kg/day/animal; and, 3) Lipopolysaccharide (LPS) IP injections from GD 13-18 at 20ug-70ug/kg/day per animal. Maternal blood pressure was measured by tail-cuff. Upon sacrifice, fetal and placenta weights were recorded. Placenta histomorphology was assessed using H&E sections. Placenta inflammation was determined by quantifying TNF-α levels and inflammatory gene expression. Placenta metabolic and mitochondrial health were determined by measuring mitochondrial respiration rates and placenta NAD
MeSH term(s)	Pregnancy ; Female ; Humans ; Rats ; Animals ; Pre-Eclampsia/metabolism ; Tumor Necrosis Factor-alpha ; Lipopolysaccharides ; Hypertension ; Inflammation/metabolism ; Poly I
Chemical Substances	Tumor Necrosis Factor-alpha ; Lipopolysaccharides ; Poly I (25249-22-3)
Language	English
Publishing date	2023-09-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1219205
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Article ; Online: Automated detection of microscopic placental features indicative of maternal vascular malperfusion using machine learning.

Patnaik, Purvasha / Khodaee, Afsoon / Vasam, Goutham / Mukherjee, Anika / Salsabili, Sina / Ukwatta, Eranga / Grynspan, David / Chan, Adrian D C / Bainbridge, Shannon

Placenta

2023 Volume 145, Page(s) 19–26

Abstract: Introduction: Hypertensive disorders of pregnancy (HDP) and fetal growth restriction (FGR) are common obstetrical complications, often with pathological features of maternal vascular malperfusion (MVM) in the placenta. Currently, clinical placental ... ...

Abstract	Introduction: Hypertensive disorders of pregnancy (HDP) and fetal growth restriction (FGR) are common obstetrical complications, often with pathological features of maternal vascular malperfusion (MVM) in the placenta. Currently, clinical placental pathology methods involve a manual visual examination of histology sections, a practice that can be resource-intensive and demonstrates moderate-to-poor inter-pathologist agreement on diagnostic outcomes, dependant on the degree of pathologist sub-specialty training. Methods: This study aims to apply machine learning (ML) feature extraction methods to classify digital images of placental histopathology specimens, collected from cases of HDP [pregnancy induced hypertension (PIH), preeclampsia (PE), PE + FGR], normotensive FGR, and healthy pregnancies, according to the presence or absence of MVM lesions. 159 digital images were captured from histological placental specimens, manually scored for MVM lesions (MVM- or MVM+) and used to develop a support vector machine (SVM) classifier model, using features extracted from pre-trained ResNet18. The model was trained with data augmentation and shuffling, with the performance assessed for patch-level and image-level classification through measurements of accuracy, precision, and recall using confusion matrices. Results: The SVM model demonstrated accuracies of 70 % and 79 % for patch-level and image-level MVM classification, respectively, with poorest performance observed on images with borderline MVM presence, as determined through post hoc observation. Discussion: The results are promising for the integration of ML methods into the placental histopathological examination process. Using this study as a proof-of-concept will lead our group and others to carry ML models further in placental histopathology.
MeSH term(s)	Pregnancy ; Female ; Humans ; Placenta/pathology ; Pregnancy Outcome ; Retrospective Studies ; Pre-Eclampsia/pathology ; Hypertension, Pregnancy-Induced/pathology ; Fetal Growth Retardation/diagnostic imaging ; Fetal Growth Retardation/pathology
Language	English
Publishing date	2023-11-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	603951-0
ISSN	1532-3102 ; 0143-4004
ISSN (online)	1532-3102
ISSN	0143-4004
DOI	10.1016/j.placenta.2023.11.005
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Article ; Online: Early onset of aging phenotype in vascular repair by Mas receptor deficiency.

Vasam, Goutham / S, Shrinidh Joshi / Miyat, Su Yamin / Adam, Hashim / Jarajapu, Yagna P

GeroScience

2021 Volume 44, Issue 1, Page(s) 311–327

Abstract: Aging is associated with impaired vascular repair following ischemic insult, largely due to reparative dysfunctions of progenitor cells. Activation of Mas receptor (MasR) was shown to reverse aging-associated vasoreparative dysfunction. This study tested ...

Abstract	Aging is associated with impaired vascular repair following ischemic insult, largely due to reparative dysfunctions of progenitor cells. Activation of Mas receptor (MasR) was shown to reverse aging-associated vasoreparative dysfunction. This study tested the impact of MasR-deficiency on mobilization and vasoreparative functions with aging. Wild type (WT) or MasR-deficient mice (MasR
MeSH term(s)	Aging ; Animals ; Hematopoietic Stem Cell Mobilization ; Heterocyclic Compounds ; Mice ; Phenotype ; Stem Cells/physiology
Chemical Substances	Heterocyclic Compounds
Language	English
Publishing date	2021-10-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-021-00473-4
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Article ; Online: Reducing mitochondrial ribosomal gene expression does not alter metabolic health or lifespan in mice.

Reid, Kim / Daniels, Eileen G / Vasam, Goutham / Kamble, Rashmi / Janssens, Georges E / Hu, Iman M / Green, Alexander E / Houtkooper, Riekelt H / Menzies, Keir J

Scientific reports

2023 Volume 13, Issue 1, Page(s) 8391

Abstract: Maintaining mitochondrial function is critical to an improved healthspan and lifespan. Introducing mild stress by inhibiting mitochondrial translation invokes the mitochondrial unfolded protein response ( ... ...

Abstract	Maintaining mitochondrial function is critical to an improved healthspan and lifespan. Introducing mild stress by inhibiting mitochondrial translation invokes the mitochondrial unfolded protein response (UPR
MeSH term(s)	Female ; Male ; Animals ; Mice ; Longevity/genetics ; Ribosomes ; Body Composition ; Life Expectancy ; Gene Expression
Language	English
Publishing date	2023-05-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-35196-3
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Article ; Online: Mitochondrial quality control in the cardiac system: An integrative view.

Cadete, Virgilio J J / Vasam, Goutham / Menzies, Keir J / Burelle, Yan

Biochimica et biophysica acta. Molecular basis of disease

2018 Volume 1865, Issue 4, Page(s) 782–796

Abstract: Recent studies have led to the discovery of multiple mitochondrial quality control (mQC) processes that operate at various scales, ranging from the degradation of proteins by mitochondrial proteases to the degradation of selected cargos or entire ... ...

Abstract	Recent studies have led to the discovery of multiple mitochondrial quality control (mQC) processes that operate at various scales, ranging from the degradation of proteins by mitochondrial proteases to the degradation of selected cargos or entire organelles in lysosomes. While the mechanisms governing these mQC processes are progressively being delineated, their role and importance remain unclear. Converging evidence however point to a complex system whereby multiple and partly overlapping processes are recruited to orchestrate a cell type specific mQC response that is adapted to the physiological state and level of stress encountered. Knowledge gained from basic model systems of mQC therefore need to be integrated within organ-specific (patho)physiological frameworks. Building on this notion, this article focuses on mQC in the heart, where developmental metabolic reprogramming, sustained contraction, and multiple pathophysiological conditions pose broadly different constraints. We provide an overview of current knowledge of mQC processes, and discuss their implication in cardiac mQC under normal and diseased conditions.
MeSH term(s)	Animals ; Humans ; Mitochondria, Heart/metabolism ; Myocardium/metabolism ; Oxidative Stress ; Peptide Hydrolases/metabolism ; Proteostasis
Chemical Substances	Peptide Hydrolases (EC 3.4.-)
Language	English
Publishing date	2018-11-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2018.11.018
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Article ; Online: Proteomics characterization of mitochondrial-derived vesicles under oxidative stress.

Vasam, Goutham / Nadeau, Rachel / Cadete, Virgilio J J / Lavallée-Adam, Mathieu / Menzies, Keir J / Burelle, Yan

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2021 Volume 35, Issue 4, Page(s) e21278

Abstract: Mitochondria share attributes of vesicular transport with their bacterial ancestors given their ability to form mitochondrial-derived vesicles (MDVs). MDVs are involved in mitochondrial quality control and their formation is enhanced with stress and may, ...

Abstract	Mitochondria share attributes of vesicular transport with their bacterial ancestors given their ability to form mitochondrial-derived vesicles (MDVs). MDVs are involved in mitochondrial quality control and their formation is enhanced with stress and may, therefore, play a potential role in mitochondrial-cellular communication. However, MDV proteomic cargo has remained mostly undefined. In this study, we strategically used an in vitro MDV budding/reconstitution assay on cardiac mitochondria, followed by graded oxidative stress, to identify and characterize the MDV proteome. Our results confirmed previously identified cardiac MDV markers, while also revealing a complete map of the MDV proteome, paving the way to a better understanding of the role of MDVs. The oxidative stress vulnerability of proteins directed the cargo loading of MDVs, which was enhanced by antimycin A (Ant-A). Among OXPHOS complexes, complexes III and V were found to be Ant-A-sensitive. Proteins from metabolic pathways such as the TCA cycle and fatty acid metabolism, along with Fe-S cluster, antioxidant response proteins, and autophagy were also found to be Ant-A sensitive. Intriguingly, proteins containing hyper-reactive cysteine residues, metabolic redox switches, including professional redox enzymes and those that mediate iron metabolism, were found to be components of MDV cargo with Ant-A sensitivity. Last, we revealed a possible contribution of MDVs to the formation of extracellular vesicles, which may indicate mitochondrial stress. In conclusion, our study provides an MDV proteomics signature that delineates MDV cargo selectivity and hints at the potential for MDVs and their novel protein cargo to serve as vital biomarkers during mitochondrial stress and related pathologies.
MeSH term(s)	Animals ; Cell Line ; Gene Expression Regulation ; Mitochondria, Heart/physiology ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Myoblasts ; Oxidative Stress ; Proteomics ; Rats ; Transport Vesicles/physiology
Chemical Substances	Mitochondrial Proteins
Language	English
Publishing date	2021-03-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202002151R
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Article ; Online: Impaired Mobilization of Vascular Reparative Bone Marrow Cells in Streptozotocin-Induced Diabetes but not in Leptin Receptor-Deficient db/db Mice.

Vasam, Goutham / Joshi, Shrinidh / Jarajapu, Yagna P R

Scientific reports

2016 Volume 6, Page(s) 26131

Abstract: Diabetes is associated with impaired mobilization of bone marrow stem/progenitor cells that accelerate vascularization of ischemic areas. This study characterized mobilization of vascular reparative bone marrow progenitor cells in mouse models of ... ...

Abstract	Diabetes is associated with impaired mobilization of bone marrow stem/progenitor cells that accelerate vascularization of ischemic areas. This study characterized mobilization of vascular reparative bone marrow progenitor cells in mouse models of diabetes. Age-matched control or streptozotocin (STZ)-induced diabetic, and db/db mice with lean-controls were studied. Mobilization induced by G-CSF, AMD3100 or ischemia was evaluated by flow cytometric enumeration of circulating Lin(-)Sca-1(+)cKit(+) (LSK) cells, and by colony forming unit (CFU) assay. The circulating WBCs and LSKs, and CFUs were reduced in both models with a shorter duration (10-12 weeks) of diabetes compared to their respective controls. Longer duration of STZ-diabetes (≥20 weeks) induced impairment of G-CSF- or AMD3100-mobilization (P < 0.01, n = 8). In db/db mice, mobilization by G-CSF or AMD3100 was either increased or unaffected (P < 0.05, n = 6 to 8). Proliferation, migration, and ischemia-induced mobilization, of LSK cells were impaired in both models. Leptin receptor antagonist, PESLAN-1, increased G-CSF- or AMD3100-mobilization of WBCs and LSKs, compared to the untreated. Leptin increased basal WBCs, decreased basal and AMD3100-mobilized LSK cells, and had no effect on G-CSF. These results suggest that mobilopathy is apparent in STZ-diabetes but not in db/db mice. Leptin receptor antagonism would be a promising approach for reversing diabetic bone marrow mobilopathy.
MeSH term(s)	Animals ; Bone Marrow Cells/physiology ; Cell Movement ; Cell Proliferation ; Colony-Forming Units Assay ; Diabetes Mellitus, Experimental/pathology ; Flow Cytometry ; Mice ; Neovascularization, Physiologic ; Receptors, Leptin/deficiency ; Stem Cells/physiology
Chemical Substances	Receptors, Leptin ; leptin receptor, mouse
Language	English
Publishing date	2016-05-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep26131
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Article: Dietary Cocoa Flavanols Enhance Mitochondrial Function in Skeletal Muscle and Modify Whole-Body Metabolism in Healthy Mice

Daussin, Frédéric Nicolas / Cuillerier, Alexane / Touron, Julianne / Bensaid, Samir / Melo, Bruno / Al Rewashdy, Ali / Vasam, Goutham / Menzies, Keir J. / Harper, Mary-Ellen / Heyman, Elsa / Burelle, Yan

Nutrients. 2021 Sept. 29, v. 13, no. 10

2021

Abstract: Mitochondrial dysfunction is widely reported in various diseases and contributes to their pathogenesis. We assessed the effect of cocoa flavanols supplementation on mitochondrial function and whole metabolism, and we explored whether the mitochondrial ... ...

Abstract	Mitochondrial dysfunction is widely reported in various diseases and contributes to their pathogenesis. We assessed the effect of cocoa flavanols supplementation on mitochondrial function and whole metabolism, and we explored whether the mitochondrial deacetylase sirtuin-3 (Sirt3) is involved or not. We explored the effects of 15 days of CF supplementation in wild type and Sirt3⁻/⁻ mice. Whole-body metabolism was assessed by indirect calorimetry, and an oral glucose tolerance test was performed to assess glucose metabolism. Mitochondrial respiratory function was assessed in permeabilised fibres and the pyridine nucleotides content (NAD⁺ and NADH) were quantified. In the wild type, CF supplementation significantly modified whole-body metabolism by promoting carbohydrate use and improved glucose tolerance. CF supplementation induced a significant increase of mitochondrial mass, while significant qualitative adaptation occurred to maintain H₂O₂ production and cellular oxidative stress. CF supplementation induced a significant increase in NAD⁺ and NADH content. All the effects mentioned above were blunted in Sirt3⁻/⁻ mice. Collectively, CF supplementation boosted the NAD metabolism that stimulates sirtuins metabolism and improved mitochondrial function, which likely contributed to the observed whole-body metabolism adaptation, with a greater ability to use carbohydrates, at least partially through Sirt3.
Keywords	calorimetry ; flavanols ; glucose ; glucose tolerance ; glucose tolerance tests ; lung function ; mitochondria ; oxidative stress ; pathogenesis ; pyridine nucleotides ; sirtuins ; skeletal muscle
Language	English
Dates of publication	2021-0929
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13103466
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: HDAC1/2 inhibitor therapy improves multiple organ systems in aged mice.

Tammaro, Alessandra / Daniels, Eileen G / Hu, Iman M / 't Hart, Kelly C / Reid, Kim / Juni, Rio P / Butter, Loes M / Vasam, Goutham / Kamble, Rashmi / Jongejan, Aldo / Aviv, Richard I / Roelofs, Joris J T H / Aronica, Eleonora / Boon, Reinier A / Menzies, Keir J / Houtkooper, Riekelt H / Janssens, Georges E

iScience

2023 Volume 27, Issue 1, Page(s) 108681

Abstract: Aging increases the risk of age-related diseases, imposing substantial healthcare and personal costs. Targeting fundamental aging mechanisms pharmacologically can promote healthy aging and reduce this disease susceptibility. In this work, we employed ... ...

Abstract	Aging increases the risk of age-related diseases, imposing substantial healthcare and personal costs. Targeting fundamental aging mechanisms pharmacologically can promote healthy aging and reduce this disease susceptibility. In this work, we employed transcriptome-based drug screening to identify compounds emulating transcriptional signatures of long-lived genetic interventions. We discovered compound 60 (Cmpd60), a selective histone deacetylase 1 and 2 (HDAC1/2) inhibitor, mimicking diverse longevity interventions. In extensive molecular, phenotypic, and bioinformatic assessments using various cell and aged mouse models, we found Cmpd60 treatment to improve age-related phenotypes in multiple organs. Cmpd60 reduces renal epithelial-mesenchymal transition and fibrosis in kidney, diminishes dementia-related gene expression in brain, and enhances cardiac contractility and relaxation for the heart. In sum, our two-week HDAC1/2 inhibitor treatment in aged mice establishes a multi-tissue, healthy aging intervention in mammals, holding promise for therapeutic translation to promote healthy aging in humans.
Language	English
Publishing date	2023-12-12
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108681
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