Data from: TNFAIP9 protects against the development of the early stage of chronic kidney disease: Focus on inflammation and fibrosis

Overexpression of TNFAIP9 resulted in the remission of renal impairment, a decreased inflammatory response, and a reduced expression of fibrotic markers. In vitro, human renal tubular epithelial human kidney-2 (HK-2) cells were exposed to tumor necrosis factor-alpha (TNF-α) or transforming growth factor-beta (TGF-β) to simulate inflammatory and fibrotic conditions, respectively. Then, the overexpression plasmid or small interfering RNA (siRNA) targeting TNFAIP9 was transfected into HK-2 cells to either overexpress or knock down the target protein.

Overexpression of TNFAIP9 reduced the TNF-α-induced inflammatory response, while its knockdown amplified it. Likewise, overexpression of TNFAIP9 decreased the TGF-β-induced fibrosis, whereas its knockdown heightened it. In summary, it is suggested that TNFAIP9 plays a protective role against the early stage of CKD by suppressing renal inflammation and fibrosis.

Therefore, targeting TNFAIP9 could be a promising therapeutic approach for CKD.