Volume 45

  • No. 4 April 2024

    Cover Credit: Lonicerin (LCR), a bioactive compound found in plants of the Lonicera japonica species, exhibits anti-inflammatory and antioxidant activities. However, the effect of LCR on wound healing under diabetes and the specific mechanism of LCR's effect has not been covered. In this study, we discovered for the first time that LCR has a potent ability to promote cell autophagy and identified the upstream regulatory protein Sirt1 as a potential target for LCR. Additionally, our results indicate that LCR can promote angiogenesis, cell migration, and anti-apoptosis, which may have implications for other research areas such as skin flap survival, In this studycerebral ischemia and reperfusion, and intestinal epithelial injury healing. Doi:10.1038/s41401-023-01193-5. See the article in pages 815–830

  • No. 3 March 2024

    Cover Credit: PANoptosis is a new type of cell death featured with pyroptosis, apoptosis and necroptosis as a result of PANoptosome formation. The core components of PANoptosome are CASP8 and RIPK3. The picture is a fluorescence microscopic visualization of the PANoptosome formed in macrophages which can be inhibited by inhibitors of reverse electron transport. Doi: 10.1038/s41401-023-01182-8. See the article in pages 594–608

  • No. 2 February 2024

    Cover Credit: Schematic illustration of possible mechanisms contributing to curcumin against desipramine-induced apoptosis and insulin secretion impairment. Curcumin could inhibit the binding of AKAP150 to PP2B and the phosphorylation of synapsin 1 induced by desipramine, and suppress desipramine-induced insulin secretion impairment. Moreover, curcumin could inhibit desipramine-induced apoptosis through PI3K/AKT/FOXO1 signaling pathway. (DOI 10.1038/s41401-023-01176-6). See the article in pages 327–338

  • No. 1 January 2024

    Cover Credit: DZ2002, a reversible inhibitor of type III S-adenosyl-L-homocysteine hydrolase, attenuates TNF-α-induced NF-κB signaling by suppressing the degradation and phosphorylation of IκB, along with NF-κB p65 phosphorylation and nuclear translocation. Additionally, DZ2002 inhibits the activation of molecules in the STAT3-PI3K-Akt pathway, suppressing the secretion of inflammatory cytokines and pro-angiogenic factors. These findings strongly support DZ2002's promising therapeutic potential for dry eye disease (DED).