CD38-Cyclic ADP-Ribose Signal System in Physiology, Biochemistry, and Pathophysiology.
Level 5 - mechanism / opinion, no new human data
Narrative review describing biochemical mechanisms and animal/disease models without systematic review methodology.
PubMed 35457121 · doi:10.3390/ijms23084306
What was done
This narrative review synthesizes biochemical and molecular biological literature on the CD38-cyclic ADP-ribose (cADPR) signaling pathway, its regulation of intracellular calcium mobilization, and its role in human diseases and animal models.
What was found
The abstract details the mechanistic pathway: CD38 synthesizes cADPR from NAD+, which triggers calcium release from the endoplasmic reticulum via ryanodine receptor channels regulated by FK506-binding protein 12.6, influencing processes like insulin secretion. The abstract reports no numerical findings or quantitative effect sizes.
Why it matters
It provides a conceptual framework linking CD38-dependent NAD+ metabolism and calcium mobilization to cell physiology and disease mechanisms.
Limits
As a narrative review, it contains no new empirical data or systematic search protocol. No quantitative data, sample sizes, or study counts are reported in the abstract.
Cited by
- supports ADP-ribosyl cyclases consume NAD to release calcium from intracellular stores such as the endoplasmic reticulum for signaling.