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Intravascular Delivery of Biologics to the Rat Kidney
Published on: September 1, 2016
Thrombospondin in renal disease
Christian Hugo1, Christoph Daniel
1Department of Nephrology and Hypertension, University Erlangen-Nürnberg, Erlangen, Germany. Christian.Hugo@rzmail.uni-erlangen.de
Nephron. Experimental Nephrology
|February 3, 2009
Summary
Thrombospondins (TSPs) regulate kidney disease processes. TSP-1 promotes fibrosis and inflammation, while TSP-2 shows anti-inflammatory and anti-proliferative effects in renal injury models.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Thrombospondins (TSPs) are matricellular glycoproteins regulating key cellular processes.
- The TSP family has five members; TSP-1 and TSP-2 roles in renal disease are studied.
- TSPs are minimally expressed in healthy kidneys but increase during renal disease.
Purpose of the Study:
- To review and compare the roles of TSP-1 and TSP-2 in renal disease pathophysiology.
- To elucidate the distinct and overlapping functions of TSP-1 and TSP-2 in kidney injury.
Main Methods:
- Analysis of existing data from various animal models of renal disease.
- Comparison of reported effects of TSP-1 and TSP-2 on renal pathophysiological changes.
Main Results:
- TSP-1 activates transforming growth factor-beta (TGF-beta), leading to profibrotic effects and inflammation.
- TSP-2 does not activate TGF-beta and exhibits anti-inflammatory and anti-proliferative properties.
- Both TSP-1 and TSP-2 are angiogenesis inhibitors, with TSP-2's effects more consistently demonstrated.
Conclusions:
- TSP-1 and TSP-2 play significant, often contrasting, roles in the progression of renal disease.
- TSP-1 appears to exacerbate kidney injury through profibrotic and inflammatory mechanisms.
- TSP-2 may offer protective effects against renal damage via anti-inflammatory and anti-proliferative actions.
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