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From Cells to Animals: Connexin43 Suppression Enhances Autophagic Flux to Restore Odontogenesis in Inflamed Dental Pulp
1 Introduction Dental pathologies primarily originate from microbial infections, where pathogens adhere to tooth surfaces, erode enamel and dentine, and subsequently trigger inflammatory responses in pulp tissue to eliminate invading microorganisms. Concurrently, this inflammatory cascade activates odontogenic differentiation of dental pulp cells, facilitating tertiary dentine formation as a defensive barrier against microbial infiltration and preserving the integrity of underlying healthy pulp.
Cross-talk between CD38 and TTP Is Essential for Resolution of Inflammation during Microbial Sepsis
Highlights • CD38 induces TTP in the onset of acute inflammation • TTP-dependent degradation of CD38 activates Sirt1 at the onset of resolution • TTP controls the resolution of inflammation during sepsis • Carbon monoxide inhibits inflammation in sepsis by increasing TTP expression Summary The resolution phase of acute inflammation is essential for tissue homeostasis, yet the underlying mechanisms remain unclear.
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