PMID- 28434143
OWN - NLM
STAT- MEDLINE
DCOM- 20170913
LR  - 20211204
IS  - 1539-0829 (Electronic)
IS  - 1534-4827 (Print)
IS  - 1534-4827 (Linking)
VI  - 17
IP  - 6
DP  - 2017 Jun
TI  - The mTOR Signaling Pathway in Myocardial Dysfunction in Type 2 Diabetes Mellitus.
PG  - 38
LID - 10.1007/s11892-017-0865-4 [doi]
AB  - PURPOSE OF REVIEW: T2DM (type 2 diabetes mellitus) is a risk factor for heart 
      failure. The mTOR (mechanistic target of rapamycin) is a key mediator of the 
      insulin signaling pathway. We will discuss the role of mTOR in myocardial 
      dysfunction in T2DM. RECENT FINDINGS: In T2DM, chronically activated mTOR induces 
      multiple pathological events, including a negative feedback loop that suppresses 
      IRS (insulin receptor substrate)-1. While short-term treatment with rapamycin, an 
      mTOR inhibitor, is a promising strategy for cardiac diseases such as acute 
      myocardial infarction and cardiac hypertrophy in T2DM, there are many concerns 
      about chronic usage of rapamycin. Two mTOR complexes, mTORC1 and mTORC2, affect 
      many molecules and processes via distinct signaling pathways that regulate 
      cardiomyocyte function and survival. Understanding mechanisms underlying 
      mTOR-mediated pathophysiological features in the heart is essential for 
      developing effective therapies for cardiac diseases in the context of T2DM.
FAU - Suhara, Tomohiro
AU  - Suhara T
AD  - Department of Anatomy, Biochemistry & Physiology, John A. Burns School of 
      Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, 
      HI, 96813, USA.
AD  - Department of Anesthesiology, Keio University School of Medicine, Tokyo, Japan.
FAU - Baba, Yuichi
AU  - Baba Y
AD  - Department of Anatomy, Biochemistry & Physiology, John A. Burns School of 
      Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, 
      HI, 96813, USA.
AD  - Department of Cardiology and Geriatrics, Kochi Medical School, Kochi University, 
      Kochi, Japan.
FAU - Shimada, Briana K
AU  - Shimada BK
AD  - Department of Anatomy, Biochemistry & Physiology, John A. Burns School of 
      Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, 
      HI, 96813, USA.
FAU - Higa, Jason K
AU  - Higa JK
AD  - Department of Anatomy, Biochemistry & Physiology, John A. Burns School of 
      Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, 
      HI, 96813, USA.
FAU - Matsui, Takashi
AU  - Matsui T
AD  - Department of Anatomy, Biochemistry & Physiology, John A. Burns School of 
      Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, 
      HI, 96813, USA. tmatsui@hawaii.edu.
LA  - eng
GR  - T32 HL115505/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Diab Rep
JT  - Current diabetes reports
JID - 101093791
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Diabetes Mellitus, Type 2/*complications/metabolism
MH  - Heart Diseases/etiology/*metabolism
MH  - Humans
MH  - Myocardium/metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC8219468
MID - NIHMS1712616
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Cell signaling
OT  - Diabetes mellitus
OT  - Heart failure
OT  - Rapamycin
OT  - mTOR
COIS- Conflict of Interest Tomohiro Suhara, Yuichi Baba, Briana K. Shimada, Jason K. 
      Higa, and Takashi Matsui declare that they have no conflict of interest.
EDAT- 2017/04/24 06:00
MHDA- 2017/09/14 06:00
PMCR- 2021/06/22
CRDT- 2017/04/24 06:00
PHST- 2017/04/24 06:00 [entrez]
PHST- 2017/04/24 06:00 [pubmed]
PHST- 2017/09/14 06:00 [medline]
PHST- 2021/06/22 00:00 [pmc-release]
AID - 10.1007/s11892-017-0865-4 [pii]
AID - 10.1007/s11892-017-0865-4 [doi]
PST - ppublish
SO  - Curr Diab Rep. 2017 Jun;17(6):38. doi: 10.1007/s11892-017-0865-4.