Bacterial infection is the main cause of apical periodontitis (AP) of teeth. This process is closely accompanied by the cell necroptosis and the release of inflammatory substances. Cell necroptosis plays multiple roles during the AP process, from limiting bacterial infection and promoting tissue healing to facilitating bacterial dissemination and aggravating tissue destruction. Understanding these different roles of necroptosis could provide new clues for developing treatment strategies of AP.

Starch-binding domain-containing protein 1 (STBD1) is a glycogen-binding protein that is pivotal to glycogen transport and metabolism and consists of a hydrophobic N-terminal, a glycogen-binding C-terminal, and two specific motifs. STBD1 is mainly found in skeletal muscle, cardiac muscle, and liver, and its subcellular localization is mainly found in the endoplasmic reticulum, mitochondria-associated membranes, and Golgi apparatus. STBD1 is involved in biological processes such as glycophagy, glycogen accumulation, and lipid droplet formation, as well as in the pathogenesis of cardiovascular diseases, metabolic diseases, and cancer.

We found that human left gastroepiploic artery (HLGA) and uterine artery (HUA) produced vasomotion that was activated by stretch, Ca²⁺ and Cl⁻ channels (TMEM16A-Ca²⁺-activated Cl⁻ channel). Vasomotion of HLGA and HUA was negatively regulated by metabolic inhibition (NaCN) via activation of ATP-sensitive K⁺ channel (K_ATP channel) which was composed of K_ir6.1, K_ir6.2, and SUR2B subunits. Physiologically, vasomotion was inhibited by the application of neuropeptides such as vasoactive inhibitory peptide and/or CRGRP. c-Kit positive protein was identified and the role of this protein in HLGA and HUA will be studied in the future. These results suggest that myogenic vasomotion of HLGA and HUA will reveal other avenues by which it may be possible to treat circulation-related human diseases.

We identified APP1, DNPEP, LAP3, LNPEP, METAP1, METAP2, PSA, and RNPEPL1 as the aminopeptidases that are required for the myogenic differentiation of C2C12 myoblasts. Especially, the suppression of LAP3 inhibited proteasomal proteolysis and promotes the myogenic differentiation of C2C12 myoblasts through AKT/TFE3/Myogenin pathways.

A softer matrix is more likely to maintain neovascularization homeostasis through autophagy.

Autophagic activation restores compression-suppressed cementoblast mineralization, which helps to restrain force-induced external root resorption. Autophagy mediates cementoblast mineralization through periostin/β-catenin axis, in which periostin plays a role in modulating the stability of β-catenin.

Ultraviolet B irradiation promotes global N6-methyladenosine (m⁶A) modification in melanocytes and upregulates METTL3, which increases the expression level of YAP1 through m⁶A modification, thereby activating the co-transcription factor TEAD1 and promoting melanogenesis.