As there
is no current effective treatment to cure WS, many clinical trials and
researches are ongoing. (Bagley, et.al, 2010) stated that genome instability, increased
pro-oxidant state, and frequent replication fork stalling are likely to trigger
intracellular stress in WS cells; these also shortened the replicative lifespan
with implicated p38 MAPK signalling. Researchers have found out that by using p38
MAPK inhibitor in collaboration with microwave heating techniques to treat WS
fibroblasts revealed an unexpected reversal of the accelerated ageing
phenotype. Thus, they have drawn a conclusion that by treating WS with p38
inhibition is likely to provide new revelations into biological mechanisms
operating in cellular senescence and human again in the future.

9.2 Vitamin C as a Treatment
in Werner’s Syndrome

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Another future treatment was suggested by (Li, et.al, 2016). The
researchers have indicated the premature aging in WS mainly affected tissues
derived from mesoderm and affected by WRN-deficient human mesenchymal stem
cells (MSCs). They found out that Vitamin C restored in-vivo viability of MSCs
in mouse model and reversed many features in premature ageing associated with
WS including cell growth arrest, increased reactive oxygen species levels,
telomere attrition, excessive secretion of inflammatory factors, as well as the
disorganisation of nuclear lamina and heterochromatin. They explained these
findings by RNA sequencing analysis that Vitamin C altered the expression of a
series of genes which involved in DNA replication, cell cycle regulation,
chromatin condensation, and DNA repairing process.  Thus, they have drawn a conclusion that Vitamin
C holds the potential as a future treatment in WS as a rejuvenated factor of WRN-deficient
human MSCs.