Zobrazeno 1 - 10
of 27
pro vyhledávání: '"Anastassia, Todor"'
Publikováno v:
Journal of Molecular and Cellular Cardiology. 42:150-158
We used isolated cardiomyocytes to investigate a possible role of mitochondrial permeability transition pore in mitochondrial abnormalities associated with heart failure. Cardiomyocytes were isolated from LV myocardium of normal control dogs and dogs
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::49eaf93229e7244d3d9156a6cce055a0
https://doi.org/10.1016/j.yjmcc.2006.09.013
https://doi.org/10.1016/j.yjmcc.2006.09.013
Publikováno v:
Heart Failure Reviews. 10:297-303
In the setting of chronic heart failure (HF), progressive left ventricular (LV) dysfunction and chamber remodeling may be due, in part, to altered expression and disorganization of cytoskeletal, linkage and extracellular proteins. This brief review d
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bb608d22e109f7e0f3c4f3fe492b2b89
https://doi.org/10.1007/s10741-005-7544-2
https://doi.org/10.1007/s10741-005-7544-2
Autor:
Pervaiz A. Chaudhry, Sharad Rastogi, Anastassia Todor, Takayuki Mishima, Hani N. Sabbah, Sudhish Mishra, Albertas I. Undrovinas, Elaine J. Tanhehco, George Suzuki, Victor G. Sharov, Ramesh C Gupta
Publikováno v:
Circulation Research. 93:1095-1101
Passive mechanical containment of failing left ventricle (LV) with the Acorn Cardiac Support Device (CSD) was shown to prevent progressive LV dilation in dogs with heart failure (HF) and increase ejection fraction. To examine possible mechanisms for
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::870cc099d33d3657d33204941aad1166
https://doi.org/10.1161/01.res.0000101932.70443.fe
https://doi.org/10.1161/01.res.0000101932.70443.fe
Autor:
Victor G. Sharov, Hideaki Morita, Elaine J. Tanhehco, Anastassia Todor, Hani N. Sabbah, George Suzuki
Publikováno v:
European Journal of Heart Failure. 5:121-129
Background: Apoptosis may contribute to the myocardial dysfunction associated with heart failure (HF). Activation of the p38 MAPK cascade can induce apoptosis in non-cardiac cells through increased expression of Fas-L, or through decreased expression
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::77cdff28175853decd772d5030d99f9a
https://doi.org/10.1016/s1388-9842(02)00254-4
https://doi.org/10.1016/s1388-9842(02)00254-4
Autor:
Victor G. Sharov, Sidney Goldstein, Pervaiz A. Chaudhry, Elaine J. Tanhehco, Anastassia Todor, Hani N. Sabbah, Takayuki Mishima, George Suzuki, Sharad Rostogi, Omar Nass, Petros V. Anagnostopoulos, Ramesh C Gupta
Publikováno v:
British Journal of Pharmacology. 138:301-309
1. We examined the effects of eprosartan, an AT(1) receptor antagonist, on the progression of left ventricular (LV) dysfunction and remodelling in dogs with heart failure (HF) produced by intracoronary microembolizations (LV ejection fraction, EF 30
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::b9f653d58baa6e6ba21a8b83e79fa56d
https://doi.org/10.1038/sj.bjp.0705032
https://doi.org/10.1038/sj.bjp.0705032
Autor:
Anastassia Todor, Ellen G. McMahon, Sidney Goldstein, Hideaki Morita, Victor G. Sharov, George Suzuki, Elaine J. Tanhehco, Hani N. Sabbah, Amy E. Rudolph, Takayuki Mishima
Publikováno v:
Circulation. 106:2967-2972
Background— In heart failure (HF), aldosterone has been implicated in the formation of reactive interstitial fibrosis, a maladaptation that contributes to left ventricular (LV) remodeling. Eplerenone is a novel selective aldosterone blocker. The pr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0319429a6271ca1dd5d14f4d3e832ebb
https://doi.org/10.1161/01.cir.0000039104.56479.42
https://doi.org/10.1161/01.cir.0000039104.56479.42
Autor:
Takayuki Mishima, Victor G. Sharov, George Suzuki, Sidney Goldstein, Anastassia Todor, Mitsuhiro Tanimura, Elaine J. Tanhehco, Hani N. Sabbah
Publikováno v:
Cardiovascular Drugs and Therapy. 16:209-214
Background. The diuretic actions of endogenously produced atrial natriuretic factor (ANF) may be beneficial in the treatment of chronic heart failure (CHF). Neutral endopeptidase (NEP) is the primary enzyme responsible for the degradation of ANF. The
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9daf3f9c466d3181cadaeb61952c6dbf
https://doi.org/10.1023/a:1020644304771
https://doi.org/10.1023/a:1020644304771
Publikováno v:
Heart failure reviews. 10(4)
Background: We previously showed that mitochondrial respiratory function is abnormal in dogs with chronic heart failure (HF). Mitochondrial permeability transition pores (MPTP) can affect mitochondrial inner membrane potential (Δ m) and mitochondria
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::06087f9d911974fb509ea5c3cfafc61f
https://pubmed.ncbi.nlm.nih.gov/16583179
https://pubmed.ncbi.nlm.nih.gov/16583179
Autor:
Victor G. Sharov, Sanjaya Khanal, Hideaki Morita, Sidney Goldstein, Makoto Imai, George Suzuki, Timothy P. O'Neill, Anastassia Todor, Sharad Rastogi, Hani N. Sabbah
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 290(6)
Matrix metalloproteinases (MMPs) contribute to the progression of left ventricular (LV) dysfunction and remodeling associated with heart failure (HF). The present study examined the long-term effects of a selective MMP inhibitor PG-530742 (PG) on the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::14e7bcd1b2235cb1ab20b0612c7d4e7d
https://pubmed.ncbi.nlm.nih.gov/16428338
https://pubmed.ncbi.nlm.nih.gov/16428338
Publikováno v:
Heart failure reviews. 10(2)
Progressive left ventricular (LV) dilation in the setting of heart failure is associated with increased mortality and morbidity. The Acorn Cardiac Support Device (CSD, Acorn Cardiovascular, Inc., St. Paul, MN) is a preformed polyester device that is
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c143aa8041ce290a246783bc9ad61a39
https://pubmed.ncbi.nlm.nih.gov/16258721
https://pubmed.ncbi.nlm.nih.gov/16258721