Derived from the neural crest, dental stem cells (DSCs) are a population of cells with the characteristics of mesenchymal stem-ness, which under certain appropriate conditions can differentiate into multiple cells such as osteocytes, chondrocytes, hepatocyte and neuronal-like cells. DSCs are consist of odontogenic stem cells mainly include dental pulp stem cells, periodontal ligament stem cells, stem cells from deciduous teeth, stem cells from apical papilla, as well as dental follicle progenitor cells. DSCs have been widely used in the field of regenerative medicine research and preclinical research, including nervous system diseases, oral diseases, immune diseases, heart and lung diseases, etc. This review will focus on the storage of DSCs and current translational and clinical studies regarding DSCs in tissue regeneration.

Cell therapy based on mesenchymal stem cells (MSCs) has been a hot research topic in recent years, including the traditional cell therapy strategy based on living cells and the new cell-free therapy strategy based on soluble proteins or bioactive molecules such as extracellular vesicles (EVs). At present, MSC-induced cells have mature functions and specific structures, and insitu transplantation combined with biomaterials or organic technology has greatly improved the settlement rate and function. On the other hand, as the large-scale culture technique and EVs separation technique evolve, it is possible to obtain a large number of pure EVs, and EVs are gradually becoming a hot spot of current research. An increasing number of studies have shown that the therapeutic effect of MSCs not only occurs by implantation and differentiation but also manifests as the paracrine effect of MSCs. In this review, we discuss the emerging outcomes of cell therapies and acellular therapies to alleviate these pathological conditions.

With the increasing understanding of mesenchymal stem cells (MSCs), their potential in tissue engineering and regenerative medicine has attracted more attention. However, some important problems need to be solved before clinical application, such as low amplification efficiency, inconsistent cell product quality, and unsatisfactory survival rate at the receptor site. Telomeres act as a clock, and they shorten when cells divide. The main mechanism for reversing telomere length is telomerase. Furthermore, telomerase is involved in antioxidation, antiapoptosis, immunological modulation, and other noncanonical processes in addition to proliferation-related tasks. Therefore, it is necessary to understand the telomere biology and telomerase of MSCs to improve their proliferation, performance stability, and antiscavenging ability. This review summarizes the progress of telomerase biological function and mechanism in MSCs, and discusses the current situation and deficiency of telomerase-related application in MSCs.

Autophagy has been extensively studied and occurs in many biological settings. However, a question remains as to whether ischemia enhances Beclin-1/LC3-Ⅱ-dependent macroautophagy in vascular endothelial cells, as has been previously thought. Furthermore, the effect of the level of autophagy on cell or skin flap survival still requires elucidation. We created a lethal ischemia model in human umbilical vascular endothelial cells (HUVECs), performed quantitative proteomics and bioinformatics analyses, and verified the autophagic status and effect both in vitro and in vivo. The significantly upregulated proteins encoded by autophagy-related genes (ATGs) included ATG2A, ATG3, ATG4B, ATG5, ATG7, ATG9A, ATG12, ATG16, and ATG101. The significantly enhanced lysosomal proteins were cathepsin B, cathepsin D, lysosome-associated membrane protein 1 (LAMP1), and LAMP2. However, the differentially expressed proteins excluded Beclin-1, microtubule-associated protein light chain 3 (LC3)-Ⅰ, and LC3-Ⅱ. Western blot analyses verified that the protein expression levels of Beclin-1, LC3-Ⅰ, and LC3-Ⅱ were neither upregulated nor downregulated in ischemia-challenged HUVECs. The autophagic status was not enhanced by rapamycin in ischemic HUVECs but appeared to be inhibited by chloroquine. Our in vivo study on rats showed that a downregulation in autophagic status jeopardized skin flap survival. In conclusion, Ischemia neither enhanced nor inhibited Beclin-1/LC3-Ⅱ-dependent canonical macroautophagy both in vitro and in vivo, in contradiction to previous studies. An appropriate autophagic homeostasis can minimize cell or skin flap damage.