Raghvendra K. Dubey

Catecholamines block the antimitogenic effect of estradiol on human glomerular mesangial cells.

Tibolone and its metabolites induce antimitogenesis in human coronary artery smooth muscle cells: role of estrogen, progesterone, and androgen receptors.

Catecholamines block the antimitogenic effect of estradiol on human coronary artery smooth muscle cells.

Hormone replacement therapy and cardiovascular disease: what went wrong and where do we go from here?

Cytochromes 1A1/1B1- and catechol-O-methyltransferase-derived metabolites mediate estradiol-induced antimitogenesis in human cardiac fibroblast.

Vascular consequences of menopause and hormone therapy: importance of timing of treatment and type of estrogen.

Adenosine inhibits PDGF-induced growth of human glomerular mesangial cells via A(2B) receptors.

2-Methoxyestradiol: a potential treatment for multiple proliferative disorders.

Medroxyprogesterone abrogates the inhibitory effects of estradiol on vascular smooth muscle cells by preventing estradiol metabolism.

Potential vascular actions of 2-methoxyestradiol.

Resveratrol, a red wine constituent, blocks the antimitogenic effects of estradiol on human female coronary artery smooth muscle cells.

Adenosine Attenuates Human Coronary Artery Smooth Muscle Cell Proliferation by Inhibiting Multiple Signaling Pathways That Converge on Cyclin D.

2-Methoxyestradiol blocks the RhoA/ROCK1 pathway in human aortic smooth muscle cells.

2-Methoxyestradiol, an endogenous 17β-estradiol metabolite, inhibits microglial proliferation and activation via an estrogen receptor-independent mechanism.

2-Methoxyestradiol: A 17β-Estradiol Metabolite With Gender-Independent Therapeutic Potential.

Mechanism of 17β-estradiol stimulated integration of human mesenchymal stem cells in heart tissue.