| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Shilpa Rani, Pradeep Kumar Sreenivasaiah, Jin Ock Kim, Mi Young Lee, Wan Seok Kang, Yong Sook Kim, Youngkeun Ahn, Woo Jin Park, Chunghee Cho, Do Han Ki. Tauroursodeoxycholic acid (TUDCA) attenuates pressure overload-induced cardiac remodeling by reducing endoplasmic reticulum stress. PloS one. vol 12. issue 4. 2017-09-07. PMID:28426781. |
microarray analysis followed by gene ontology (go) and pathway analysis demonstrated that extracellular matrix genes responsible for hypertrophy and fibrosis, and mitochondrial genes responsible for apoptosis and fatty acid metabolism were significantly altered in the veh-tac group, but the alterations were normalized in the tudca-tac group, suggesting potential of tudca in treatment of heart diseases related to pressure-overload. |
2017-09-07 |
2023-08-13 |
mouse |
| Rajendra Ragho. An 'Omics' Perspective on Cardiomyopathies and Heart Failure. Trends in molecular medicine. vol 22. issue 9. 2017-08-29. PMID:27499035. |
unbiased omics studies have begun to provide a glimpse into the molecular framework underpinning altered mechanotransduction, mitochondrial energetics, oxidative stress, and extracellular matrix in the heart undergoing physiological and pathological hypertrophy. |
2017-08-29 |
2023-08-13 |
Not clear |
| Vanessa Pellegrinelli, Stefania Carobbio, Antonio Vidal-Pui. Adipose tissue plasticity: how fat depots respond differently to pathophysiological cues. Diabetologia. vol 59. issue 6. 2017-08-28. PMID:27039901. |
wat is characterised by its capacity to adapt and expand in response to surplus energy through processes of adipocyte hypertrophy and/or recruitment and proliferation of precursor cells in combination with vascular and extracellular matrix remodelling. |
2017-08-28 |
2023-08-13 |
Not clear |
| Gordon A Begg, Arun V Holden, Gregory Y H Lip, Sven Plein, Muzahir H Tayebje. Assessment of atrial fibrosis for the rhythm control of atrial fibrillation. International journal of cardiology. vol 220. 2017-08-28. PMID:27389440. |
fibrosis causes an increase in volume of dysfunctional extracellular matrix, and is associated with cellular alterations such as hypertrophy, apoptosis and membrane dysfunction within the atrial myocardium. |
2017-08-28 |
2023-08-13 |
Not clear |
| Adrian Santos-Ledo, Marina Garcia-Macia, Philip D Campbell, Marta Gronska, Florence L Marlo. Kinesin-1 promotes chondrocyte maintenance during skeletal morphogenesis. PLoS genetics. vol 13. issue 7. 2017-08-22. PMID:28715414. |
initial cartilage specification is intact; however, during remodeling, kif5blof chondrocytes die and the cartilage matrix devoid of hypertrophic chondrocytes remains and impedes normal ossification. |
2017-08-22 |
2023-08-13 |
zebrafish |
| Tatsuki Enoshiri, Motoko Naitoh, Satoko Yamawaki, Atsushi Kawaguchi, Rino Aya, Kazuo Noda, Yasuhiro Katayama, Takahiro Doi, Tetsuma Kawaji, Shigehiko Suzuk. β-Adrenergic Receptor Blockers Reduce the Occurrence of Keloids and Hypertrophic Scars after Cardiac Device Implantation: A Single-Institution Case-Control Study. Plastic and reconstructive surgery. vol 139. issue 5. 2017-08-17. PMID:28092339. |
keloids and hypertrophic scars are characterized by excessive proliferation of fibroblasts; abnormal accumulation of extracellular matrix; and clinical findings of raised, red, itchy, and painful lesions. |
2017-08-17 |
2023-08-13 |
Not clear |
| Timothy P Rutkowski, Anat Kohn, Deepika Sharma, Yinshi Ren, Anthony J Mirando, Matthew J Hilto. HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development. Journal of cell science. vol 129. issue 11. 2017-08-08. PMID:27160681. |
rbpjκ-dependent notch signaling regulates multiple processes during cartilage development, including chondrogenesis, chondrocyte hypertrophy and cartilage matrix catabolism. |
2017-08-08 |
2023-08-13 |
Not clear |
| Timothy P Rutkowski, Anat Kohn, Deepika Sharma, Yinshi Ren, Anthony J Mirando, Matthew J Hilto. HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development. Journal of cell science. vol 129. issue 11. 2017-08-08. PMID:27160681. |
hey1 and heyl play no discernable role in regulating chondrogenesis or chondrocyte hypertrophy, whereas none of the hes or hey factors appear to mediate notch regulation of cartilage matrix catabolism. |
2017-08-08 |
2023-08-13 |
Not clear |
| Christopher S Fry, Tyler J Kirby, Kate Kosmac, John J McCarthy, Charlotte A Peterso. Myogenic Progenitor Cells Control Extracellular Matrix Production by Fibroblasts during Skeletal Muscle Hypertrophy. Cell stem cell. vol 20. issue 1. 2017-07-26. PMID:27840022. |
myogenic progenitor cells control extracellular matrix production by fibroblasts during skeletal muscle hypertrophy. |
2017-07-26 |
2023-08-13 |
Not clear |
| Christopher S Fry, Tyler J Kirby, Kate Kosmac, John J McCarthy, Charlotte A Peterso. Myogenic Progenitor Cells Control Extracellular Matrix Production by Fibroblasts during Skeletal Muscle Hypertrophy. Cell stem cell. vol 20. issue 1. 2017-07-26. PMID:27840022. |
satellite cells, the predominant stem cell population in adult skeletal muscle, are activated in response to hypertrophic stimuli and give rise to myogenic progenitor cells (mpcs) within the extracellular matrix (ecm) that surrounds myofibers. |
2017-07-26 |
2023-08-13 |
Not clear |
| Hiroe Toba, Presley L Cannon, Andriy Yabluchanskiy, Rugmani Padmanabhan Iyer, Jeanine D'Armiento, Merry L Lindse. Transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis. American journal of physiology. Heart and circulatory physiology. vol 312. issue 3. 2017-07-26. PMID:28011588. |
transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis. |
2017-07-26 |
2023-08-13 |
mouse |
| Carlos A Roncal-Jimenez, Takuji Ishimoto, Miguel A Lanaspa, Tamara Milagres, Ana Andres Hernando, Thomas Jensen, Makoto Miyazaki, Tomohito Doke, Takahiro Hayasaki, Takahiko Nakagawa, Shoichi Marumaya, David A Long, Gabriela E Garcia, Masanari Kuwabara, Laura G Sánchez-Lozada, Duk-Hee Kang, Richard J Johnso. Aging-associated renal disease in mice is fructokinase dependent. American journal of physiology. Renal physiology. vol 311. issue 4. 2017-07-24. PMID:27465991. |
the renal injury was amplified by provision of high-salt diet for 3 wk, as noted by the presence of glomerular hypertrophy, mesangial matrix expansion, and alpha smooth muscle actin expression, and with segmental thrombi. |
2017-07-24 |
2023-08-13 |
mouse |
| Albert S Chang, Catherine K Hathaway, Oliver Smithies, Masao Kakok. Transforming growth factor-β1 and diabetic nephropathy. American journal of physiology. Renal physiology. vol 310. issue 8. 2017-06-29. PMID:26719364. |
tgf-β1 promotes cell hypertrophy and extracellular matrix accumulation in the mesangium, which decreases glomerular filtration rate and leads to chronic renal failure. |
2017-06-29 |
2023-08-13 |
Not clear |
| Esmé Jansen van Vuren, Leoné Malan, Roland von Känel, Marike Cockeran, Nicolaas T Mala. Hyperpulsatile pressure, systemic inflammation and cardiac stress are associated with cardiac wall remodeling in an African male cohort: the SABPA study. Hypertension research : official journal of the Japanese Society of Hypertension. vol 39. issue 9. 2017-06-29. PMID:27169396. |
cardiac remodeling is characterized by myocyte hypertrophy, myocyte death and modifications of the extracellular matrix. |
2017-06-29 |
2023-08-13 |
Not clear |
| b' Terezie Pelik\\xc3\\xa1nov\\xc3\\xa. [Diabetic retinopathy: pathogenesis and therapeutic implications]. Vnitrni lekarstvi. vol 62. issue 7-8. 2017-06-26. PMID:27627088.' |
these activated cells change the production pattern of a number of mediators such as growth factors, proinflammatory cytokines, vasoactive molecules, coagulation factors and adhesion molecules resulting in increased blood flow, increased capillary permeability, proliferation of extracellular matrix and thickening of basal membranes, altered cell turnover (apoptosis, proliferation, hypertrophy), procoagulant and proaggregant pattern, and finally in angiogenesis and tissue remodelling. |
2017-06-26 |
2023-08-13 |
Not clear |
| Regina Irwin, Sandi Raehtz, Narayanan Parameswaran, Laura R McCab. Intestinal inflammation without weight loss decreases bone density and growth. American journal of physiology. Regulatory, integrative and comparative physiology. vol 311. issue 6. 2017-06-26. PMID:27733383. |
in addition, we observed a reduction in growth plate thickness and hypertrophic chondrocyte matrix components (collagen x). |
2017-06-26 |
2023-08-13 |
mouse |
| X Zhang, W-J Huang, W-W Che. TGF-β1 factor in the cerebrovascular diseases of Alzheimer's disease. European review for medical and pharmacological sciences. vol 20. issue 24. 2017-06-26. PMID:28051272. |
however, related to the pathological features of ad, the brain overexpression of tgf-β1 was associated with neuroinflammation, accumulation of extracellular matrix compounds and cerebrovascular stiffness, neuronal apoptosis along with the development of vascular hypertrophy. |
2017-06-26 |
2023-08-13 |
mouse |
| Shutong Shen, Huimin Jiang, Yihua Bei, Junjie Xiao, Xinli L. Long Non-Coding RNAs in Cardiac Remodeling. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. vol 41. issue 5. 2017-06-23. PMID:28376483. |
lncrnas including chaer, chast, mhrt, chrf, ror, h19, and miat have been implicated in cardiac hypertrophy while nrf, h19, apf, carl, uca, mhrt and several other lncrnas (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. |
2017-06-23 |
2023-08-13 |
Not clear |
| Meriam Nefla, Dirk Holzinger, Francis Berenbaum, Claire Jacque. The danger from within: alarmins in arthritis. Nature reviews. Rheumatology. vol 12. issue 11. 2017-06-22. PMID:27733758. |
in oa, high mobility group protein b1 (hmgb1) and s100 proteins, along with many other alarmins, are abundantly secreted by joint cells, promoting cartilage matrix catabolism, osteophyte formation, angiogenesis and hypertrophic differentiation. |
2017-06-22 |
2023-08-13 |
Not clear |
| Yona Goldshmit, Sari Schokoroy Trangle, Fabian Afergan, Tal Iram, Ronit Pinkas-Kramarsk. Nucleolin inhibitor GroA triggers reduction in epidermal growth factor receptor activation: Pharmacological implication for glial scarring after spinal cord injury. Journal of neurochemistry. vol 138. issue 6. 2017-06-13. PMID:27399849. |
reactive astrocytes become hypertrophic, proliferate and secrete chondroitin sulphate proteoglycans into the extracellular matrix (ecm). |
2017-06-13 |
2023-08-13 |
Not clear |