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Glutathione and cardiovascular diseases

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Cardiovascular disease (CDV) is the number 1 cause of death globally, taking an estimated 18 million lives each year. Whilst an increased risk of CDV is often genetic in origin, the effect of negative lifestyle choices such as excessive alcohol consumption, smoking and poor diet play a well documented role in the development of CVD.

Complications in the cardiovascular system arise from elevated levels of free radicals which cause tissue damage and interrupt cellular signalling mechanisms [1]. Apart from lifestyle choices, there is a wide range of medical conditions that, by their nature, produce excessive free radicals, including diabetes, hypertension, stroke, and obesity. Whilst small bouts of increased levels of free radicals is normal, indeed required for signalling purposes and immune responses, it is the oxidative stress caused by sustained and excessive free radical production that leads to deleterious health outcomes [2].

Means to prevent this sustained damage caused by oxidative stress have been studies extensively and are of major therapeutic interest [3]. Whilst there is an abundance of pharmacological means to control chronic diseases such as diabetes or hypertension, reducing excessive production of free radicals from all possible sources presents a major challenge.

As the principal intracellular antioxidant, Glutathione has been extensively researched. This interest stems from numerous studies into chronic diseases in which elevated levels of free radicals cause sustained oxidative stress. Glutathione acts directly by scavenging free radicals and several studies have reported that patients with heart disease have lower levels of glutathione. Furthermore, a reduction of glutathione levels was also reported in subjects with asymptomatic CVD, which suggest that measuring and supplementing glutathione levels may help detect and treat such cases early. [1-9]

References

  1. Bajic, V.P., et al., Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease. Oxid Med Cell Longev, 2019. 2019: p. 5028181.
  2. Goszcz, K., et al., Antioxidants in Cardiovascular Therapy: Panacea or False Hope? Front Cardiovasc Med, 2015. 2: p. 29.
  3. Li, H.G., S. Horke, and U. Forstermann, Oxidative stress in vascular disease and its pharmacological prevention. Trends in Pharmacological Sciences, 2013. 34(6): p. 313-319.
  4. van der Pol, A., et al., Treating oxidative stress in heart failure: past, present and future. Eur J Heart Fail, 2019. 21(4): p. 425-435.
  5. Mistry, R.K. and A.C. Brewer, Redox-Dependent Regulation of Sulfur Metabolism in Biomolecules: Implications for Cardiovascular Health. Antioxid Redox Signal, 2019. 30(7): p. 972-991.
  6. Kanaan, G.N. and M.E. Harper, Cellular redox dysfunction in the development of cardiovascular diseases. Biochim Biophys Acta Gen Subj, 2017. 1861(11 Pt A): p. 2822-2829.
  7. Go, Y.-M. and D.P. Jones, Cysteine/cystine redox signaling in cardiovascular disease. Free Radical Biology and Medicine, 2011. 50(4): p. 495-509.
  8. Houston, M.C., Nutraceuticals, Vitamins, Antioxidants, and Minerals in the Prevention and Treatment of Hypertension. Progress in cardiovascular diseases, 2005. 47(6): p. 396-449.
  9. Mills, B.J., et al., Blood glutathione and cysteine changes in cardiovascular disease. Journal of Laboratory & Clinical Medicine, 2000. 135(5): p. 396-401.

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