Abstract
Diabetic nephropathy (DN) presents with a gradual breakdown of the glomerular filtration barrier to protein, culminating in widespread glomerular damage and renal failure. The podocyte is the central cell of the glomerular filtration barrier, and possesses unique architectural and signaling properties guided by the expression of key podocyte specific proteins. How these cellular features are damaged by the diabetic milieu is unclear, but what is becoming increasingly clear is that damage to the podocyte is a central event in DN. Here we present accumulating evidence that insulin action itself is important in podocyte biology, and may be deranged in the pathomechanism of early DN. This introduces a rationale for therapeutic intervention to improve podocyte insulin sensitivity early in the presentation of DN.
| Original language | English |
|---|---|
| Pages (from-to) | 22-7 |
| Number of pages | 6 |
| Journal | Current Diabetes Reviews |
| Volume | 7 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2011 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Animals
- Diabetic Nephropathies/metabolism
- Glucose/adverse effects
- Humans
- Insulin/metabolism
- Insulin Resistance/physiology
- Models, Biological
- Podocytes/drug effects
- Proteinuria/metabolism
- Signal Transduction/drug effects
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