Neuropathy and inflammation in diabetic bone marrow
Jiyin Zhou1, Zuo Zhang1, Guisheng Qian2
1National Drug Clinical Trial Institution, The Second Affiliated Hospital, Army Medical University, Chongqing, China.
Diabetes/Metabolism Research and Reviews
|October 6, 2018
Summary
Diabetes harms bone marrow (BM) stem cell function and regeneration. Therapies targeting BM stem cells show promise for treating diabetic neuropathy by improving neurotrophic and angiogenic effects.
Area of Science:
- Regenerative Medicine
- Diabetology
- Neuroscience
Background:
- Diabetes mellitus significantly impairs bone marrow (BM) architecture and function, affecting stem cell mobilization and regenerative capacity.
- Diabetic neuropathy is linked to reduced sympathetic nerve endings in the BM, disrupting circadian regulation of immature cell migration via beta-adrenergic receptors.
- Existing research highlights the role of BM stem cells in ameliorating diabetic neuropathy through secreted factors and immune modulation.
Purpose of the Study:
- To investigate the role of bone marrow (BM) stem cells in the context of diabetic neuropathy.
- To explore the therapeutic potential of targeting BM stem cells for improving diabetic neuropathy and its associated BM dysfunction.
- To identify key mechanisms by which BM stem cells exert therapeutic effects in diabetic neuropathy.
Main Methods:
- Review of existing literature on diabetes, bone marrow function, diabetic neuropathy, and stem cell therapy.
- Analysis of the molecular and cellular interactions between BM stem cells and the diabetic microenvironment.
- Examination of the role of neurotrophic factors, growth factors, adipokines, and macrophage polarization in therapeutic outcomes.
Main Results:
- Diabetes-induced BM dysfunction is characterized by impaired stem cell function and reduced regenerative potential.
- Mesenchymal stem cells, BM mononuclear cells, hematopoietic stem cells, and stromal cells can ameliorate diabetic neuropathy-associated dysfunction.
- Therapeutic effects are mediated by secreted factors (neurotrophic, growth factors, adipokines) and modulation of macrophage M2 polarization and inflammation.
Conclusions:
- Bone marrow stem cell dysfunction is a critical component of diabetic neuropathy.
- Targeting BM stem cells offers a novel therapeutic strategy for diabetic neuropathy, addressing both angiogenic and neurotrophic deficits.
- Modulating inflammation via BM stem cells presents a potential therapeutic avenue for improving diabetic neuropathy.
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