MTORC1-Regulated Metabolism Controlled by TSC2 Limits Cardiac Reperfusion Injury.

ABSTRACT:

Rationale

The mTORC1 (mechanistic target of rapamycin complex-1) controls metabolism and protein homeostasis and is activated following ischemia reperfusion (IR) injury and by ischemic preconditioning (IPC). However, studies vary as to whether this activation is beneficial or detrimental, and its influence on metabolism after IR is little reported. A limitation of prior investigations is their use of broad gain/loss of mTORC1 function, mostly applied before ischemic stress. This can be circumvented by regulating one serine (S1365) on TSC2 (tuberous sclerosis complex) to achieve bidirectional mTORC1 modulation but only with TCS2-regulated costimulation.

Objective

We tested the hypothesis that reduced TSC2 S1365 phosphorylation protects the myocardium against IR and is require

SUBMITTER: Oeing CU 

PROVIDER: S-EPMC8257748 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature