"Iron chelators against venous leg ulcers and multiple sclerosis"

Hypothetical molecular mechanisms by which local iron overload
facilitates the development of venous leg ulcers and multiple
sclerosis lesions. [JOURNAL ARTICLE]
Med Hypotheses 2008 Apr 7.
Simka M, Rybak Z

This paper presents a hypothetical model of role for iron in the
development of venous leg ulcers and multiple sclerosis.
Elevated concentrations of iron were found in the skin affected by
venous hypertension and also in the areas of brain with multiple
sclerosis lesions.
Individuals with hemochromatosis gene (HFE) mutations: C282Y and H63D,
which result in a less efficient transport of iron by macrophages, are
characterized by an increased risk for venous leg ulcer and multiple
sclerosis.
Multiple sclerosis is a T cell-mediated disease, and T cells probably
participate in the development of venous ulcers.
This deleterious role of ferric ions could be related to the
regulation of T cell proliferation and apoptosis.
Under normal conditions excessive accumulation of T cells cannot take
place, because nitric oxide and interferon-gamma drive these cells
toward apoptosis.
However, in tissues with a high concentration of iron, T lymphocytes
proliferate instead of undergoing apoptosis.
This is possible due to the internalization of the INF-gammaR2 chain
of the interferon-gamma receptor, the downregulation of inducible
nitric oxide synthase expression in macrophages and the inactivation
of the active site of caspases.
Yet, it should be emphasized that this hypothesis does not claim for
the increased concentration of iron as a direct causal factor for the
development of venous ulcerations or multiple sclerosis, but rather,
iron is a factor that modulates and exaggerates the autoimmune
process.
Iron chelators, administered systemically or locally, should
potentially exhibit therapeutic and prophylactic activity against
venous leg ulcers and multiple sclerosis.
Medical hypotheses [Med Hypotheses]
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