PMID- 21320507
OWN - NLM
STAT- MEDLINE
DCOM- 20110926
LR  - 20211203
IS  - 1095-8584 (Electronic)
IS  - 0022-2828 (Print)
IS  - 0022-2828 (Linking)
VI  - 50
IP  - 6
DP  - 2011 Jun
TI  - Three 4-letter words of hypertension-related cardiac hypertrophy: TRPC, mTOR, and 
      HDAC.
PG  - 964-71
LID - 10.1016/j.yjmcc.2011.02.004 [doi]
AB  - Left ventricular hypertrophy due to hypertension represents a major risk factor 
      for adverse cardiovascular events and death. In recent years, the prevalence of 
      cardiac hypertrophy has increased due to obesity and an aging population. 
      Notably, a significant number of individuals have persistent cardiac hypertrophy 
      in the face of blood pressure that is normalized by drug treatment. Thus, a 
      better understanding of the processes underlying the cardiac remodeling events 
      that are set into play by hypertension is needed. At the level of the cardiac 
      myocytes, hypertrophic growth is often described as physiological, as occurs with 
      exercise, or pathological, as seen with hypertension. Here we discuss recent 
      developments in three areas that are fundamental to pathological hypertrophic 
      growth of cardiac myocytes. These areas are the transient receptor potential 
      canonical (TRPC) channels, mammalian target of rapamycin (mTOR) complexes, and 
      histone deacetylase (HDAC) enzymes. In the last several years, studies in each of 
      these areas have yielded new and exciting discoveries into the genesis of 
      pathological growth of cardiac myocytes. The phosphoinositide 3-kinase-Akt 
      signaling network may be the common denominator that links these areas together. 
      Defining the interrelationship among TRPC channels, mTOR signaling, and HDAC 
      enzymes is a promising, but challenging area of research. Such knowledge will 
      undoubtedly lead to new drugs that better prevent or reverse left ventricular 
      hypertension.
CI  - Copyright (c) 2011 Elsevier Ltd. All rights reserved.
FAU - Kurdi, Mazen
AU  - Kurdi M
AD  - Department of Chemistry and Biochemistry, Faculty of Sciences, Lebanese 
      University, Rafic Hariri Educational Campus, Hadath, Lebanon.
FAU - Booz, George W
AU  - Booz GW
LA  - eng
GR  - R01 HL088101-02S1/HL/NHLBI NIH HHS/United States
GR  - R01 HL088101-04/HL/NHLBI NIH HHS/United States
GR  - R01HL088101-02S1/HL/NHLBI NIH HHS/United States
GR  - R01HL088101-04/HL/NHLBI NIH HHS/United States
GR  - R01 HL088101/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20110219
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - 0 (TRPC Cation Channels)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Animals
MH  - Cardiomegaly/*etiology/*physiopathology
MH  - Histone Deacetylases/*metabolism
MH  - Humans
MH  - Hypertension/*complications/*physiopathology
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - TRPC Cation Channels/*metabolism
PMC - PMC3091951
MID - NIHMS273736
COIS- Disclosures The authors have no conflicts of interest to disclose.
EDAT- 2011/02/16 06:00
MHDA- 2011/09/29 06:00
PMCR- 2012/06/01
CRDT- 2011/02/16 06:00
PHST- 2010/12/07 00:00 [received]
PHST- 2011/01/26 00:00 [revised]
PHST- 2011/02/02 00:00 [accepted]
PHST- 2011/02/16 06:00 [entrez]
PHST- 2011/02/16 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
PHST- 2012/06/01 00:00 [pmc-release]
AID - S0022-2828(11)00065-4 [pii]
AID - 10.1016/j.yjmcc.2011.02.004 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 2011 Jun;50(6):964-71. doi: 10.1016/j.yjmcc.2011.02.004. Epub 
      2011 Feb 19.