TABLE 2.

Physiological and pathological implications in kidney of PPAR-null mice for the different isotypes.

Isotypes of PPAR-null mice	Physiological and pathological implication
PPARα-null	• PPARα-null mice exhibited significantly greater kidney dysfunction after I/R injury, as assessed by higher serum creatinine levels and enhanced tubular necrosis Portilla et al. (2000)
	• PPARα-null mice had worse kidney function and metabolic derangement in experimental polymicrobial sepsis. Tissue mRNA expression of markers of kidney injury and inflammation were more elevated. Expression of enzymes associated with FAO and fatty acid transport was lower Iwaki et al. (2019)
	• Diabetic PPARα-null mice exhibited increased blood glucose, HbA1c, serum free fatty acid and triglyceride levels, and a persistent increase in urine albumin excretion. The increase in type IV collagen and TGF-β in the glomeruli were more prominent in diabetic PPARα-null mice Panchapakesan et al. (2004)
	• Aged PPARα null mice showed reduced expression of FAO-associated proteins and genes, higher lipid accumulation, vacuoles in tubules compared to control littermates Chung et al. (2018)
PPARβ-null	• PPARβ-null mice developed more severe ischemic acute renal failure than wild-type mice. Epithelial cell sloughing was more extensive in PPARβ-null mice, leading to tubular dilation and cast formation Lee et al, (2011)
	• PPARβ/δ-null female mice showed impairment of apoptotic cell clearance and reduction in anti-inflammatory cytokine production. These mice were much more likely to develop autoimmune kidney disease, a lupus-like autoimmunity Mukundan et al. (2009)
PPARγ-null	• PPARγ null mice showed increased glucosuria and albuminuria. With age, the mice developed renal insufficiency, advance of type 2 diabetes, and APS Toffoli et al. (2017)
	• The proximal tubular epithelial cells PPAR-γ deletions mice developed more severe tubulointerstitial fibrosis Zhao et al, (2016)