X
Search Filters
Format Format
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
chemistry (17) 17
index medicus (17) 17
metallurgy (16) 16
treatment of water, waste water, sewage, or sludge (16) 16
animals (13) 13
performing operations (12) 12
physical or chemical processes or apparatus in general (12) 12
separation (12) 12
transporting (12) 12
mice (11) 11
heart failure (9) 9
autophagy (8) 8
cardiac & cardiovascular systems (8) 8
cell biology (7) 7
cells (7) 7
humans (6) 6
mitochondria (6) 6
apoptosis (5) 5
heart (5) 5
inflammation (5) 5
male (5) 5
myocardium - pathology (5) 5
pressure-overload (5) 5
article (4) 4
biochemistry & molecular biology (4) 4
cardiovascular (4) 4
mitochondrial dna (4) 4
myocardium - metabolism (4) 4
physiological aspects (4) 4
proteins (4) 4
signal transduction (4) 4
autophagy-related protein 5 (3) 3
biological phenomena, cell phenomena, and immunity (3) 3
cardiomyocytes (3) 3
cell death (3) 3
cytokines (3) 3
degradation (3) 3
heart failure - enzymology (3) 3
heart failure - etiology (3) 3
heart failure - metabolism (3) 3
heart-failure (3) 3
hypertrophy (3) 3
mice, inbred c57bl (3) 3
mice, knockout (3) 3
microtubule-associated proteins - metabolism (3) 3
mitophagy (3) 3
multidisciplinary sciences (3) 3
myocardium - enzymology (3) 3
myocytes, cardiac - metabolism (3) 3
oxidative stress (3) 3
peripheral vascular disease (3) 3
phosphorylation (3) 3
protein (3) 3
rodents (3) 3
toll-like receptor 9 (3) 3
ablation (2) 2
activation (2) 2
analysis (2) 2
aorta - pathology (2) 2
binding (2) 2
biochemistry (2) 2
biology (2) 2
biophysics (2) 2
calcium (2) 2
calpain (2) 2
calpain - metabolism (2) 2
cardiomegaly - pathology (2) 2
cardiomegaly - physiopathology (2) 2
cardiomyopathies - metabolism (2) 2
cell growth (2) 2
cell-growth (2) 2
cytokines - genetics (2) 2
death (2) 2
development and progression (2) 2
disease (2) 2
domestic plumbing installations for fresh water or waste water (2) 2
dysfunction (2) 2
enzyme activation - drug effects (2) 2
failure (2) 2
fixed constructions (2) 2
gene expression regulation - physiology (2) 2
genetic aspects (2) 2
heart - physiopathology (2) 2
heart failure - pathology (2) 2
hematology (2) 2
hemic and lymphatic diseases (2) 2
hemodynamic stress (2) 2
immune system diseases (2) 2
inhibition (2) 2
mice, transgenic (2) 2
microtubule-associated proteins - genetics (2) 2
mitochondria, heart - metabolism (2) 2
myocardial-infarction (2) 2
myocytes, cardiac - enzymology (2) 2
myocytes, cardiac - pathology (2) 2
neoplasms (2) 2
nf-kappa b - metabolism (2) 2
organ specificity - drug effects (2) 2
parkin (2) 2
physiology (2) 2
more...
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Nature, ISSN 0028-0836, 05/2012, Volume 484, Issue 7397, pp. 251 - 255
Journal Article
Journal Article
Cell Reports, ISSN 2211-1247, 01/2019, Volume 26, Issue 2, pp. 338 - 345.e6
Degradation of mitochondria by selective autophagy, termed mitophagy, contributes to the control of mitochondrial quality. Bcl2-L-13 is a mammalian homolog of... 
Bcl2-L-13 | Atg32 | mitophagy | mitochondria | PROTEIN ATG8 | KINASE | GENES | CYTOPLASM | AUTOPHAGOSOME FORMATION | BINDING | CELL BIOLOGY
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2016, Volume 11, Issue 3, p. e0152628
Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell growth, proliferation and metabolism. mTORC1 regulates protein synthesis positively... 
MAMMALIAN TARGET | RHEB GTPASE | RAPAMYCIN | GENE | MULTIDISCIPLINARY SCIENCES | TSC2 | PROLIFERATION | MICE | CELL-GROWTH | ATP RELEASE | MODEL | Heart - physiopathology | Mitochondria, Heart - ultrastructure | Organ Specificity - drug effects | Tumor Suppressor Proteins - metabolism | Mitochondria, Heart - metabolism | TOR Serine-Threonine Kinases - metabolism | Mice, Inbred C57BL | Cardiomegaly - physiopathology | Cardiomegaly - pathology | Mitochondria, Heart - drug effects | Down-Regulation - drug effects | Enzyme Activation - drug effects | Autophagy - drug effects | Mechanistic Target of Rapamycin Complex 1 | Up-Regulation - drug effects | Multiprotein Complexes - metabolism | Phenotype | Animals | Signal Transduction - drug effects | Heart - drug effects | Protein Biosynthesis - drug effects | Trehalose - pharmacology | Autophagy (Cytology) | Tuberous sclerosis | Physiological aspects | Development and progression | Genetic aspects | Mitochondrial DNA | Research | TOR protein | Heart | Tuberous sclerosis 2 protein | Brain | Phosphorylation | Trehalose | Homeostasis | Homology | Kinases | Autophagy | Protein turnover | Proteins | Signal transduction | Mitochondria | Cell growth | Misalignment | Rodents | Inhibition | Heart diseases | Abnormalities | Cardiomyocytes | Protein biosynthesis | Rapamycin | Metabolism | Organelles | Ablation | Studies | TSC2 protein | Signaling | Life span | Protein synthesis | Fibrosis | Mice | Infiltration | Mutation | Initiation factor eIF-4E | Phagocytosis | Hypertrophy | Apoptosis | Structure-function relationships
Journal Article
Journal Article
Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 07/2019
Stress is known as a risk factor for both mental and physical health problems. While stress is known as one of the major health problems in modern society, a... 
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 12/2016, Volume 311, Issue 6, pp. H1485 - H1497
We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory... 
Myocardial infarction | Cardiac fibroblast | Inflammation | Cardiac rupture | Toll-like receptor 9 | CELLS | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | cardiac fibroblast | myocardial infarction | HEART-FAILURE | DEATH | CARDIOMYOCYTES | cardiac rupture | REPAIR | INHIBITION | inflammation | DNA | PERIPHERAL VASCULAR DISEASE | TARGETED DELETION | NF-KAPPA-B | Cell Count | Actins - metabolism | Toll-Like Receptor 9 - genetics | Heart Rupture, Post-Infarction - mortality | Ki-67 Antigen - metabolism | Male | NF-kappa B - metabolism | Myocardial Infarction - diagnostic imaging | RNA, Messenger - metabolism | Heart Rupture, Post-Infarction - etiology | Cell Differentiation - genetics | Heart Rupture, Post-Infarction - immunology | Ligation | Myocardial Infarction - pathology | Myocardium - metabolism | Cytokines - genetics | Real-Time Polymerase Chain Reaction | Cell Proliferation - genetics | NF-kappa B - antagonists & inhibitors | Myocardium - pathology | Survival Rate | Myocardial Infarction - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mice, Knockout | Myofibroblasts - cytology | Myocardial Infarction - complications | Animals | Magnetic Field Therapy | Coronary Vessels - surgery | Fibroblasts - cytology | Heart Rupture, Post-Infarction - genetics | Mice | Toll-like receptors | Physiological aspects | Health aspects | Heart attack | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article
American Journal of Physiology: Heart and Circulatory Physiology, ISSN 0363-6135, 12/2016, Volume 311, Issue 6, pp. H1485 - H1485
We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory... 
Journal Article
American Journal of Physiology, ISSN 0363-6135, 12/2016, Volume 311, Issue 6, p. H1485
  We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory... 
Heart failure | Phosphorylation | Heart attacks | Cytokines | Rodents | Cells
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 07/2019, Volume 515, Issue 3, pp. 442 - 447
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2013, Volume 288, Issue 14, pp. 10176 - 10187
Journal Article