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Interactions of hyperhomocysteinemia and T cell immunity in causation of hypertension

Sudhakar Veeranki1,1, Siva K Gandhapudi1,1, Suresh C Tyagi1,1

  • 1Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.

Canadian Journal of Physiology and Pharmacology
|July 12, 2016
PubMed

Insights

High homocysteine levels (HHcy) may increase cardiovascular disease (CVD) risk, especially with inflammation and hypertension. Understanding HHcy causes, like defective remethylation or transsulfuration, is crucial for managing hypertension and CVD risk.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Metabolic Science

Background:

  • Hyperhomocysteinemia (HHcy) is an established cardiovascular disease (CVD) risk factor, but its precise role is debated.
  • Homocysteine-lowering therapies show limited efficacy in humans, unlike in animal models, suggesting population heterogeneity and epigenetic factors.
  • HHcy may contribute to CVD synergistically with other risk factors like inflammation and hypertension.

Purpose of the Study:

  • To explore the interplay between homocysteine, T cell immunity, and hypertension in CVD risk.
  • To propose a more nuanced understanding of HHcy's contribution to CVD.
  • To highlight the importance of investigating the underlying causes of HHcy.

Main Methods:

  • Review of existing literature on homocysteine, inflammation, T cell immunity, and hypertension.
  • Synthesis of evidence linking these factors to cardiovascular risk.
  • Conceptual framework development for understanding HHcy's role.

Main Results:

  • Elevated homocysteine levels are linked to increased inflammation.
  • Homocysteine, T cell immunity, and hypertension may act in concert to elevate CVD risk.
  • Defective remethylation or transsulfuration pathways may differentially impact hypertension progression.

Conclusions:

  • HHcy's role in CVD may be context-dependent, influenced by co-existing risk factors and individual genetic/epigenetic profiles.
  • Investigating the specific causes of HHcy (remethylation vs. transsulfuration defects) is essential for targeted interventions.
  • A comprehensive approach considering homocysteine metabolism, immune function, and hypertension is needed for effective CVD risk management.

Keywords:
T cellscardiovascular diseasehyperhomocysteinemiahyperhomocystéinémiehypertensioninflammationlymphocytes Tmaladie cardiovasculaire

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