Page 172 - EJMO-9-1

Eurasian Journal of Medicine and
Oncology
Key signaling proteins in cardiovascular disease

gene of interest in CVD. Mutations in GNAS have been modulation. Furthermore, mutations in GNAS disrupt
associated with various cardiovascular conditions, signal transduction pathways, impair heart function,
including pseudohypoparathyroidism, Albright hereditary and contribute to arteriosclerosis and hypertension.
osteodystrophy (AHO), and McCune–Albright syndrome In addition, TP53, widely known for its role in cancer,
(MAS). These mutations disrupt GNAS signaling is implicated in atherosclerotic plaque instability and
53
pathways, affecting multiple cardiac functions. Notably, increased cardiovascular risk. This study provides valuable
GNAS mutations have been associated with abnormalities insights into the molecular complexity of CVDs and offers
in calcium signaling, leading to arrhythmias and cardiac potential opportunities for developing targeted therapeutic
dysfunction. Furthermore, dysregulated GNAS signaling interventions to improve these critical health conditions.
54
has been implicated in the progression of arterial stiffness
and hypertension. Exploring the precise mechanisms Acknowledgments
55
by which GNAS impacts CVD may provide insights into This work is based on research supported by the Faculty
potential therapeutic targets. Finally, TP53 is a critical gene of Natural Science Research Office at University of the
involved in diverse cellular activities, including apoptosis, Western Cape. The opinions and conclusions expressed are
DNA repair, and cell cycle control. Although widely those of the author and should not necessarily be attributed
recognized for its role in cancer, accumulating evidence to the research office.
highlights its involvement in CVDs. Mutations in TP53
have been identified in atherosclerotic plaques, where they Funding
were associated with plaque instability and an increased
34
risk of cardiovascular events. Dysregulation of TP53 None.
results in the proliferation of vascular smooth muscle cells, Conflict of interest
inflammation, and oxidative stress, all of which contribute
to atherosclerosis progression. 56,57 Understanding the The author declares no conflict of interest.
interplay between TP53 and CVD could open avenues
for therapeutics targeting its downstream pathways. Author contributions
A limitation of this study is the lack of consideration for This is a single-authored article.
age and sex as contributing factors. Aging is associated
with significant structural, histological, and biochemical Ethics approval and consent to participate
changes. These alterations, even without other risk factors, Not applicable.
58
can create an environment conducive to atherosclerosis
and vascular calcification. This process involves the Consent for publication
59
activation of the bone morphogenetic protein (BMP)
signaling pathway, a key component of which includes Not applicable.
proteins from the TGF-β superfamily, the focus of the Availability of data
60
present study. Despite the limitation, these findings offer
valuable insights into the molecular mechanisms driving Data supporting the findings of this study are available
CVD and the potential therapeutic targets. from the corresponding author upon reasonable request.
5. Conclusion References

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Volume 9 Issue 1 (2025) 164 doi: 10.36922/ejmo.8086