And since resveratrol stimulates production of SIRT1, a serum that blocks diseases by speeding up the cell's energy production centers known as mitrochondria. Ask your doctor how much red wine you should be drinking to prevent such atrophy. Until we know a better way on this red wine is the obvious choice. I bet your stroke hospital will never serve red wine.
The latest here:
Muscle‐specific sirtuin1 gain‐of‐function ameliorates skeletal muscle atrophy in a pre‐clinical mouse model of cerebral ischemic stroke
First published: 21 May 2020
This article has been accepted for publication and
undergone full peer review but has not been through the copyediting,
typesetting, pagination and proofreading process, which may lead to
differences between this version and the Version of Record. Please cite
this article as doi:10.1096/fba.2020‐00017
Abstract
Stroke causes severe long‐term disability in patients due to
the induction of skeletal muscle atrophy and weakness, but the
molecular mechanisms remain elusive. Using a preclinical mouse model of
cerebral ischemic stroke, we show that stroke robustly induced atrophy
as well as significantly decreased gene expression in the PTA
(paralytic tibialis anterior) muscle. Muscle‐specific SirT1
gain‐of‐function mice are resistant to stroke‐induced muscle atrophy and
this protective effect requires its deacetylase activity. Although
SirT1 counteracts the stroke‐induced up‐regulation of atrogin1, MuRF1
and ZNF216 genes, we found a mechanism that regulates the ZNF216 gene
transcription in post‐stroke muscle. Stroke increased the expression of
the ZNF216 gene in post‐stroke TA muscle by activating PARP‐1, which
binds on the ZNF216 promoter. The SirT1 gain‐of‐function or SirT1
activator, resveratrol, reversed the PARP‐1‐mediated up‐regulation of
ZNF216 expression at the promoter level, suggesting a contradicted role
for SirT1 and PARP‐1 in the regulation of ZNF216 gene. Overall, our
study for the first‐time demonstrated that (1) stroke causes muscle
atrophy, in part, through the SirT1/PARP‐1/ZNF216 signaling mechanism,
(2) SirT1 can block muscle atrophy in response to different types of
atrophic signals via different signaling mechanisms, and (3) identified SirT1 as a critical regulator of post‐stroke muscle mass.
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