All Relations between apoptosis and hypertrophic

Publication Sentence Publish Date Extraction Date Species
Jian-Guo Wu, Li Ma, Shu-Ya Zhang, Zhan-Zhou Zhu, Hong Zhang, Lu-Ping Qin, Yan-Jie We. Essential oil from rhizomes of Ligusticum chuanxiong induces apoptosis in hypertrophic scar fibroblasts. Pharmaceutical biology. vol 49. issue 1. 2011-09-01. PMID:20815693. essential oil from rhizomes of ligusticum chuanxiong induces apoptosis in hypertrophic scar fibroblasts. 2011-09-01 2023-08-12 Not clear
Hong-Sheng Wang, Demetrios A Arvanitis, Min Dong, Paul J Niklewski, Wen Zhao, Chi Keung Lam, Evangelia G Kranias, Despina Sanoudo. SERCA2a superinhibition by human phospholamban triggers electrical and structural remodeling in mouse hearts. Physiological genomics. vol 43. issue 7. 2011-09-01. PMID:21266500. furthermore, multiple structural and transcription factor gene expression changes indicate an ongoing structural remodeling process, favoring hypertrophy and myogenesis while suppressing apoptosis and progression to heart failure. 2011-09-01 2023-08-12 mouse
Mark Luedde, Saskia Spaich, Hans-Joerg Hippe, Sebastian Busch, Rainer Will, Issam Abu-Taha, Tilman Klein, Christian Kuhn, Derk Frank, Hugo A Katus, Norbert Fre. Affixin (β-parvin) promotes cardioprotective signaling via STAT3 activation. Journal of molecular and cellular cardiology. vol 50. issue 5. 2011-08-03. PMID:21295579. in conclusion, we demonstrate that affixin activates stat3 in cardiomyocytes and promotes characteristic stat3-related effects such as hypertrophy, protection against apoptosis, and angiogenesis. 2011-08-03 2023-08-12 rat
Soojeong Kang, Elie R Chemaly, Roger J Hajjar, Djamel Lebech. Resistin promotes cardiac hypertrophy via the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) and c-Jun N-terminal kinase/insulin receptor substrate 1 (JNK/IRS1) pathways. The Journal of biological chemistry. vol 286. issue 21. 2011-07-28. PMID:21478152. these data demonstrate that resistin induces cardiac hypertrophy and myocardial insulin resistance, possibly via the ampk/mtor/p70(s6k) and apoptosis signal-regulating kinase 1/jnk/irs1 pathways. 2011-07-28 2023-08-12 rat
Josemaria Paterno, Ivan N Vial, Victor W Wong, Kristine C Rustad, Michael Sorkin, Yubin Shi, Kirit A Bhatt, Hariharan Thangarajah, Jason P Glotzbach, Geoffrey C Gurtne. Akt-mediated mechanotransduction in murine fibroblasts during hypertrophic scar formation. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 19. issue 1. 2011-07-26. PMID:21134033. in vivo inhibition of akt increased apoptosis but did not significantly abrogate hypertrophic scar development. 2011-07-26 2023-08-12 Not clear
Kang Tang, Xun Li, Ming-Qi Zheng, George J Rozansk. Role of apoptosis signal-regulating kinase-1-c-Jun NH2-terminal kinase-p38 signaling in voltage-gated K+ channel remodeling of the failing heart: regulation by thioredoxin. Antioxidants & redox signaling. vol 14. issue 1. 2011-07-18. PMID:20518594. c-jun nh(2)-terminal kinase (jnk) and p38 kinase are key regulators of cardiac hypertrophy and apoptosis during pathological stress, but their role in regulating ion channels in the diseased heart is unclear. 2011-07-18 2023-08-12 rat
Prema Robinson, Armandina Garza, Jeffrey Moore, T Kris Eckols, Skakun Parti, Vishwanathan Balaji, Jesus Vallejo, David J Tweard. Substance P is required for the pathogenesis of EMCV infection in mice. International journal of clinical and experimental medicine. vol 2. issue 1. 2011-07-14. PMID:19436834. emcv infection resulted in 51% mortality at 14 days and a 1.56 fold increase in heart-to-body weight ratio that was accompanied by cardiac inflammation and necrosis and along with cardiomyocyte apoptosis and hypertrophy of surviving cells. 2011-07-14 2023-08-12 mouse
Prema Robinson, Armandina Garza, Jeffrey Moore, T Kris Eckols, Skakun Parti, Vishwanathan Balaji, Jesus Vallejo, David J Tweard. Substance P is required for the pathogenesis of EMCV infection in mice. International journal of clinical and experimental medicine. vol 2. issue 1. 2011-07-14. PMID:19436834. in contrast, sp precursor knockout mice were completely protected from emcv-mortality, cardiomegaly, cardiac inflammation and necrosis as well as cardiomyocyte apoptosis and hypertrophy. 2011-07-14 2023-08-12 mouse
K D Evans, L E Sheppard, D I Grossman, S H Rao, R B Martin, A M Oberbaue. Long Term Cyclic Pamidronate Reduces Bone Growth by Inhibiting Osteoclast Mediated Cartilage-to-Bone Turnover in the Mouse. The open orthopaedics journal. vol 2. 2011-07-14. PMID:19572021. humeral length was decreased in pamidronate treated mice compared to vehicle control mice, and correlated with greater growth plate areas reflecting greater proliferative and hypertrophic chondrocyte cell numbers with fewer hypertrophic cells undergoing apoptosis. 2011-07-14 2023-08-12 mouse
James N Tsoporis, Forough Mohammadzadeh, Thomas G Parke. Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease. Cardiovascular psychiatry and neurology. vol 2010. 2011-07-14. PMID:20672023. forced expression of s100b in neonatal rat myocyte cultures and high level expression of s100b in transgenic mice hearts inhibit cardiac hypertrophy and the associated phenotype but augments myocyte apoptosis following myocardial infarction. 2011-07-14 2023-08-12 mouse
James N Tsoporis, Forough Mohammadzadeh, Thomas G Parke. Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease. Cardiovascular psychiatry and neurology. vol 2010. 2011-07-14. PMID:20672023. by contrast, knocking out s100b, augments hypertrophy, decreases apoptosis and preserves cardiac function following myocardial infarction. 2011-07-14 2023-08-12 mouse
Marielle Doyon, Taben Mary Hale, Julie-Emilie Huot-Marchand, Rong Wu, Jacques de Champlain, Denis DeBloi. Does atorvastatin induce aortic smooth muscle cell apoptosis in vivo? Vascular pharmacology. vol 54. issue 1-2. 2011-07-07. PMID:20951229. primary endpoints included aortic medial hypertrophy and aortic smc hyperplasia, internucleosomal dna fragmentation and expression of the apoptosis regulatory proteins bax and bcl-2. 2011-07-07 2023-08-12 rat
Yoshikazu Taketa, Akira Inomata, Satoru Hosokawa, Jiro Sonoda, Kazuhiro Hayakawa, Kyoko Nakano, Yuki Momozawa, Joji Yamate, Midori Yoshida, Toyohiko Aoki, Kazuo Tsukidat. Histopathological characteristics of luteal hypertrophy induced by ethylene glycol monomethyl ether with a comparison to normal luteal morphology in rats. Toxicologic pathology. vol 39. issue 2. 2011-07-07. PMID:21422263. although the size of cl varied, all cl in egme-treated rats had histological features similar to type ii cl, but they were more hypertrophic with less apoptosis. 2011-07-07 2023-08-12 rat
Caroline B Marshall, Ron D Krofft, Mary J Blonski, Jolanta Kowalewska, Christine M Logar, Jeffrey W Pippin, Francis Kim, Robert Feil, Charles E Alpers, Stuart J Shanklan. Role of smooth muscle protein SM22α in glomerular epithelial cell injury. American journal of physiology. Renal physiology. vol 300. issue 4. 2011-07-01. PMID:21289056. in the face of injury, podocytes may proceed along several possible pathways, including dedifferentiation and proliferation, persistent cell cycle arrest, hypertrophy, apoptosis, or necrosis. 2011-07-01 2023-08-12 mouse
Jeffrey G Dickhout, Rachel E Carlisle, Richard C Austi. Interrelationship between cardiac hypertrophy, heart failure, and chronic kidney disease: endoplasmic reticulum stress as a mediator of pathogenesis. Circulation research. vol 108. issue 5. 2011-06-27. PMID:21372294. although cardiac hypertrophy may be initially adaptive, prolonged or severe er stress resulting from the increased protein synthesis associated with cardiac hypertrophy can lead to apoptosis of cardiac myocytes and result in reduced cardiac output and chronic heart failure. 2011-06-27 2023-08-12 Not clear
M Zhong, D H Carney, H Jo, B D Boyan, Z Schwart. Inorganic phosphate induces mammalian growth plate chondrocyte apoptosis in a mitochondrial pathway involving nitric oxide and JNK MAP kinase. Calcified tissue international. vol 88. issue 2. 2011-06-22. PMID:21104071. chondrocytes in the hypertrophic zone of the growth plate undergo apoptosis during endochondral bone development via mechanisms that involve inorganic phosphate (pi) and nitric oxide (no). 2011-06-22 2023-08-12 mouse
Nicole Stieger, Kirstin Worthmann, Mario Schiffe. The role of metabolic and haemodynamic factors in podocyte injury in diabetes. Diabetes/metabolism research and reviews. vol 27. issue 3. 2011-06-16. PMID:21309047. almost all components of the diabetic milieu lead to serious podocyte stress, driving the cells towards cell cycle arrest and hypertrophy, detachment and apoptosis. 2011-06-16 2023-08-12 human
Dianne M Perez, Van A Doz. Cardiac and neuroprotection regulated by α(1)-adrenergic receptor subtypes. Journal of receptor and signal transduction research. vol 31. issue 2. 2011-06-16. PMID:21338248. this review will summarize the evidence that this dual regulation can be mediated through the different α(1)-ar subtypes in the context of cardiac hypertrophy, heart failure, apoptosis, ischemic preconditioning, neurogenesis, locomotion, neurodegeneration, cognition, neuroplasticity, depression, anxiety, epilepsy, and mental illness. 2011-06-16 2023-08-12 Not clear
Anne Margreet De Jong, Alexander H Maass, Silke U Oberdorf-Maass, Dirk J Van Veldhuisen, Wiek H Van Gilst, Isabelle C Van Gelde. Mechanisms of atrial structural changes caused by stretch occurring before and during early atrial fibrillation. Cardiovascular research. vol 89. issue 4. 2011-06-13. PMID:21075756. in this review, we describe different aspects of structural remodelling as seen in animal models and in patients with af, including atrial enlargement, cellular hypertrophy, dedifferentiation, fibrosis, apoptosis, and loss of contractile elements. 2011-06-13 2023-08-12 Not clear
Mahipal Singh, Cerrone R Foster, Suman Dalal, Krishna Sing. Role of osteopontin in heart failure associated with aging. Heart failure reviews. vol 15. issue 5. 2011-06-02. PMID:20127409. the post-mi infarct healing process involves temporarily overlapping phases that include the following--(1) inflammation with migration and adhesion of neutrophils and macrophages, phagocytosis and inflammatory gene expression; (2) tissue repair with fibroblast adhesion and proliferation, myofibroblast differentiation, extracellular matrix deposition and scar formation; and (3) structural and functional remodeling of infarcted and non-infarcted myocardium through cardiac myocyte apoptosis, hypertrophy and myocardial angiogenesis. 2011-06-02 2023-08-12 mouse