Results 51 to 60 of about 280,420 (306)

Pim3 up-regulation by YY1 contributes to diabetes-induced cardiac hypertrophy and heart failure [PDF]

open access: yesIranian Journal of Basic Medical Sciences
Objective(s): The close relationship of proto-oncogenes to myocardial hypertrophy has long been recognized, and cardiac hypertrophy leads to heart failure (HF).
Xiao Jin   +6 more
doaj   +1 more source

Determining the absolute requirement of G protein-coupled receptor kinase 5 for pathological cardiac hypertrophy: short communication. [PDF]

open access: yes, 2012
RATIONALE: Heart failure (HF) is often the end phase of maladaptive cardiac hypertrophy. A contributing factor is activation of a hypertrophic gene expression program controlled by decreased class II histone deacetylase (HDAC) transcriptional repression ...
Gao, Erhe   +4 more
core   +2 more sources

Enigma in cardiac hypertrophy [PDF]

open access: yesCardiovascular Research, 2010
The Enigma subfamily belongs to the PDZ- (for PSD-95, DLG, ZO-1) and LIM- (for LIN-11, Isl-1, MEC-3) encoding protein family. This family is composed of at least four different members: Enigma (also called PD-LIM7; LMP-1), Enigma homologue (ENH), ZASP/Cypher/Oracle, and LMP-4.
openaire   +2 more sources

Tissue Engineered Human Elastic Cartilage From Primary Auricular Chondrocytes for Ear Reconstruction

open access: yesAdvanced Functional Materials, EarlyView.
Despite over three decades of research, no tissue‐engineered solution for auricular reconstruction in microtia patients has reached clinical translation. The key challenge lies in generating functional elastic cartilage ex vivo. Here, we integrate synergistic cell‐biomaterial strategies to engineer auricular grafts with mechanical and histological ...
Philipp Fisch   +13 more
wiley   +1 more source

Inhibiting SLC26A4 reverses cardiac hypertrophy in H9C2 cells and in rats [PDF]

open access: yesPeerJ, 2020
Background It has been confirmed that mutations in solute carrier family 26 member 4 (SLC26A4) contribute to pendred syndrome. However, the role of SLC26A4 in cardiac hypertrophy and the signaling pathways remain unclear.
Liqun Tang   +3 more
doaj   +2 more sources

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes [PDF]

open access: yes, 2017
Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes ...
Bei, Roberto   +10 more
core   +2 more sources

Infusible Extracellular Matrix Biomaterial Enhances Cell‐Specific Pro‐Repair Responses Following Acute Myocardial Infarction

open access: yesAdvanced Healthcare Materials, EarlyView.
We measure the cell‐specific responses of administering infusible ECM (iECM) in acute myocardial infarction (MI) across multiple timepoints. Using single‐nucleus RNA sequencing and spatial transcriptomics, we measure macrophage activation, fibroblast remodeling, increased vascular development, lymphangiogenesis, cardioprotection, and neurogenesis ...
Joshua M. Mesfin   +18 more
wiley   +1 more source

The orphan receptor TR3 participates in angiotensin II‐induced cardiac hypertrophy by controlling mTOR signalling

open access: yesEMBO Molecular Medicine, 2012
Angiotensin II (AngII) induces cardiac hypertrophy and increases the expression of TR3. To determine whether TR3 is involved in the regulation of the pathological cardiac hypertrophy induced by AngII, we established mouse and rat hypertrophy models using
Rong‐Hao Wang   +15 more
doaj   +1 more source

Glycogen synthase kinases 3α and 3β in cardiac myocytes: regulation and consequences of their inhibition [PDF]

open access: yes, 2008
Inhibition of glycogen synthase kinase 3β (GSK3β) as a consequence of its phosphorylation by protein kinase B/Akt (PKB/Akt) has been implicated in cardiac myocyte hypertrophy in response to endothelin-1 or phenylephrine.
Alsafi, Ali   +7 more
core   +1 more source

Farnesyltransferase Deficiency in Cardiomyocytes Initiates Senescence and Contributes to Cardiac Fibrosis

open access: yesAdvanced Science, EarlyView.
Lipid overload suppresses SREBF2‐mediated FNTB expression, leading to defective Lamin A maturation and nuclear envelope instability. This nuclear catastrophe triggers a pro‐fibrotic senescence program in cardiomyocytes. Notably, restoring nuclear integrity via AAV9‐based gene therapy effectively attenuates cardiac remodeling, identifying the ...
Yuxiao Chen   +16 more
wiley   +1 more source

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