Pmaip1, also known as NoxA, is a pro-apoptotic mitochondrial protein in the B-cell lymphoma-2 (Bcl-2) family. It plays a role in apoptosis, and is involved in various biological processes and signaling pathways. Its dysregulation can have significant impacts on cell survival and disease development [3,4,6,7].

In osteoporosis, Pmaip1 was identified as a core gene. It can promote the osteogenesis, migration and proliferation of bone marrow mesenchymal stem cells (BMSCs), and was thus proposed as a potential biomarker for osteoporosis diagnosis and treatment [1]. In another study, Pmaip1 was found to suppress autophagy in osteoblasts via the AMPK/mTOR pathway, inhibiting their proliferation and differentiation, and si-PMAIP1 could inhibit the development of osteoporosis in an ovariectomy (OVX) model of rats [2].

In acute myeloid leukemia (AML), Pmaip1 knockout confirmed its major role in driving the synergy between venetoclax and 5-azacitidine, suggesting it may be a key factor in the response to this combinatorial treatment [4].

In follicular thyroid carcinoma (FTC), knockdown of Pmaip1 significantly inhibited the proliferation and metastasis of FTC cells both in vivo and in vitro, as it regulated FOSL1 by modulating the Wnt signaling pathway [5].

In acute aortic dissection (AAD), the pro-apoptotic gene Pmaip1 was highly expressed, and cannabidiol could inhibit its expression to reduce AAD-associated morbidity and mortality by suppressing macrophage infiltration and PMAIP1-induced vascular smooth muscle cell apoptosis [6].

In Alzheimer's disease, siRNA-PMAIP1 could alleviate mitochondrial dysfunction and inhibit cell apoptosis, indicating it may affect mitochondrial function in hippocampal neuronal cells [8].

In conclusion, Pmaip1 is a crucial gene involved in apoptosis and various biological processes. Studies using gene-knockout or other loss-of-function models have revealed its significant roles in diseases such as osteoporosis, AML, FTC, AAD, and Alzheimer's disease, providing valuable insights into disease mechanisms and potential therapeutic targets.