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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.