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Table 1 Timeline of significant research papers linking atherosclerosis with impaired sulfate supply to the vasculature

From: A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome

Publication

Key finding

Mann, 1960 [13]

Sulfur supplementation protects monkeys from atherosclerosis, due to dietary cholesterol and choline enrichment.

Hauss et al., 1962 [110]

Chondroitin sulfate incorporation into connective tissue is greatly enriched in the atherosclerotic aorta.

McCully, 1969 [14]

Homocysteine plays an important role in arteriosclerosis.

Bleau et al., 1974 [84]

Deficient Ch-S in RBCs leads to increased hemolysis; Ch-S stabilization of RBC membrane by SEM.

Bergner et al., 1981 [32]

Cholesterol sulfatase deficiency leads to massive accumulation of Ch-S in RBCs and plasma.

Avila et al., 1996 [37]

Chagas infection induces Ch-S autoantibodies.

Paka et al., 1999 [98]

ApoE promotes both cholesterol egress from macrophages in the plaque and sulfation of the glycocalyx.

Strott, 2003 [30]

The only review article available on Ch-S’s role in physiology.

Freitas et al., 2005 [38]

Chagas disease induces heart failure many years later; with minimal evidence of cardiovascular disease.

Ren et al., 2007 [35]

Ch-S regulates lipid metabolism in the liver.

Ma et al., 2008 [34]

Ch-S decreases lipid biosynthesis in macrophages.

Qiao et al., 2010 [141]

H2S is involved in pathogenesis of atherosclerosis.

Davidson and Seneff, 2012 [49]

Sulfate deficiency leads to decreased deformability and increased aggregation of RBCs, increased (less negative) zeta potential, and increased capillary surface tension.

Manna and Jain, 2011 [118]

H2S enhances glucose uptake by cells

Seneff et al., 2012 [16]

eNOS produces sulfate catalyzed by sunlight.

Xu et al., 2012 [33]

Ch-S suppresses inflammatory response in macrophages.

Xu et al., 2014 [142]

H2S is a promising therapy for atherosclerosis.

Toshikuni et al., 2015 [130]

Elevated serum GGT predicts carotid plaque build-up.