ALDH2 overexpression

However, ALDH2 overexpression protected proximal tubule epithelial cells from transforming growth factor-β-induced dedifferentiation or partial epithelial-mesenchymal transdifferentiation in vitro. Thus, our findings yield important clinical information regarding the development and progression of CKD involving ALDH2, especially among East Asian populations.

Additionally, the suppression of ALDH2 on IL-6 and TNF-α levels and promotion of it on OCN and RUNX2 expression in PDLSC model of periodontitis was further intensified by ferrostatin-1, but reversed by FIN56. ALDH2 may alleviate inflammation and facilitate osteogenic differentiation of PDLSC in periodontitis by hindering ferroptosis via activating Nrf2, suggesting it to be a promising candidate for treating periodontitis.

Overexpression of ALDH2 inhibited cell viability, proliferation, migration, and invasion of A375/SK-MEL-2 cells. ALDH2 is a new gene biomarker of melanoma, which exerts an inhibitory effect on melanoma.

Mechanistically, ALDH2 may cooperate with genes such as C5orf32, TSPAN8 and RILP to inhibit GC progression via regulating multiple signaling pathways and chemical carcinogenesis. Therefore, our study suggested that ALDH2, an important variant gene in Asians, might serve as a prognostic marker and a potential therapeutic target for patients with GC.

Silencing of the key targets of RNF41 attenuates the chemotherapy resistance of ALDH2 to LSCs.Conclusion : ALDH2 inhibition increases the sensitivity of leukaemia stem cells to cytarabine therapy by glucose metabolism reprogramming and redox balance. Aldh2-mediated reduction of oxidative phosphorylation, loss of quiescence and differentiation of LSCs induced by oxidative stress, play an important role in cytarabine sensitization , suggesting an alternative strategy for the treatment of AML patients.

The rescue experiments further illustrated the effects of the two on the malignant behaviors of HCC cells. Forced expression of miR-671-5p fostered the proliferation, migration and invasion of HCC cells by restraining ALDH2.