From: Pathophysiology and treatment of focal segmental glomerulosclerosis: the role of animal models
Animal models | Method of developing | Examples of FSGS research conducted using these animal models |
---|---|---|
5/6 renal mass resection | Use of thromboxane inhibitors [35] | |
Use of lipid lowering agents [36] | ||
Use of peroxisome proliferator [37] | ||
Use of antifibrotic agents [38] | ||
Absence of p21 [39] | ||
Absence of Apolipoprotein E [40] | ||
Salt sensitive animals | ||
Norepinephrine | ||
Angiotensin | ||
Zucker rats | Role of macrophage influx [43] | |
Munich Wistar rats | ||
SLE | Use of TNF-α blockade [46] | |
Adriamycin Puromycin | Use of ACE-I + Ang II inhibitors [54] | |
Role of MAPK [55] | ||
Use of CCL2 vaccination [56] | ||
Role of fibronectin as biomarker [57] | ||
Role of Rab 23 as biomarker [58] | ||
Streptozotocin | Role of good glycemic versus blood pressure control [60] | |
Vpr-gene | Use of fluvastatin [64] | |
Use of CYC202 [67] | ||
SIVAN | [65] | |
Mpv-17 | Role of mitochondrial DNA [69] | |
α-actinin 4 | Genetic human FSGS comparison [70] | |
Podocin-deficiency | ||
Thy-1. | Role of ACE-I [75] | |
hDTR | Presence of threshold [2] | |
Collapsing variant serum injection | Podocyte damage after injection [76] | |
Supernatant injection | Induction of transient proteinuria [77] | |
Spontaneously [78] | Accidental | Use of BMT [79] |
 |  | Role of QTL [80] |