Parkinson’s disease (PD) is a common neurodegenerative disorder caused by genetic, epigenetic, and environmental factors. Recent advance in genomics and epigenetics have revealed epigenetic mechanisms in PD. These epigenetic modifications include DNA methylation, post-translational histone modifications, chromatin remodeling, and RNA-based mechanisms, which regulate cellular functions in almost all cells. Epigenetic alterations are involved in multiple aspects of neuronal development and neurodegeneration in PD. In this review, we discuss current understanding of the epigenetic mechanisms that regulate gene expression and neural degeneration and then highlight emerging epigenetic targets and diagnostic and therapeutic biomarkers for treating or preventing PD.

Parkinson’s disease (PD) is one of the most common neurodegenerative disorders of aging, characterized by the degeneration of dopamine neurons (DA neurons) in the substantial nigra, leading to the advent of both motor symptoms and non-motor symptoms. Current treatments include electrical stimulation of the affected brain areas and dopamine replacement therapy. Even though both categories are effective in treating PD patients, the disease progression cannot be stopped. The research advance into cell therapies provides exciting potential for the treatment of PD. Current cell sources include neural stem cells (NSCs) from fetal brain tissues, human embryonic stem cells (hESCs), induced pluripotent stem cells (iPSCs) and directly induced dopamine neurons (iDA neurons). Here, we evaluate the research progress in different cell sources with a focus on using iPSCs as a valuable source and propose key challenges for developing cells suitable for large-scale clinical applications in the treatment of PD.

Astragalus membranaceus Bunge is widely used in Traditional Chinese Medicine to treat various cancers. Astragaloside‑IV (AS‑IV) is one of the major compounds isolated from A. membranaceus Bunge and has been demonstrated to have antitumor effects by inhibiting cell proliferation, invasion and metastasis in various cancer types. Numerous studies have used in vitro cell culture and in vivo animal models of cancer to explore the antitumor activities of AS‑IV. In the present study, the antitumor effects and mechanisms of AS‑IV reported in studies recorded in the PubMed database were reviewed. First, the antitumor effects of AS‑IV on proliferation, cell cycle, apoptosis, autophagy, invasion, migration, metastasis and epithelial‑mesenchymal transition processes in cancer cells and the tumor microenvironment, including angiogenesis, tumor immunity and macrophage‑related immune responses to cancer cells, were comprehensively discussed. Subsequently, the molecular mechanisms and related signaling pathways associated with antitumor effects of AS‑IV as indicated by in vitro and in vivo studies were summarized, including the Wnt/AKT/GSK-3β (glycogen synthase kinase‑3β)/β‑catenin, TGF‑β/PI3K/AKT/mTOR, PI3K/MAPK/mTOR, PI3K/AKT/NF‑κB, Rac family small GTPase 1/RAS/MAPK/ERK, TNF‑α/protein kinase C/ERK1/2‑NF‑κB and Tregs (T‑regulatory cells)/IL‑11/STAT3 signaling pathways. Of note, several novel mechanisms of Toll‑like receptor 4 (TLR4)/NF‑κB/STAT3, pSmad3C/3L, nuclear factor erythroid 2‑related factor (NrF2)/heme oxygenase 1, circDLST/microRNA‑489‑3p/eukaryotic translation initiation factor 4A1 and macrophage‑related high‑mobility group box 1‑TLR4 signaling pathways associated with the anticancer activity of AS‑IV were also included. Finally, the limitations of current studies that must be addressed in future studies were pointed out to facilitate the establishment of AS‑IV as a potent therapeutic drug in cancer treatment.