PMID- 37371672
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230701
IS  - 2227-9059 (Print)
IS  - 2227-9059 (Electronic)
IS  - 2227-9059 (Linking)
VI  - 11
IP  - 6
DP  - 2023 May 29
TI  - Ca(2+)-Mediated Signaling Pathways: A Promising Target for the Successful 
      Generation of Mature and Functional Stem Cell-Derived Pancreatic Beta Cells In 
      Vitro.
LID - 10.3390/biomedicines11061577 [doi]
LID - 1577
AB  - Diabetes mellitus is a chronic disease affecting over 500 million adults globally 
      and is mainly categorized as type 1 diabetes mellitus (T1DM), where pancreatic 
      beta cells are destroyed, and type 2 diabetes mellitus (T2DM), characterized by 
      beta cell dysfunction. This review highlights the importance of the divalent 
      cation calcium (Ca(2+)) and its associated signaling pathways in the proper 
      functioning of beta cells and underlines the effects of Ca(2+) dysfunction on 
      beta cell function and its implications for the onset of diabetes. Great interest 
      and promise are held by human pluripotent stem cell (hPSC) technology to generate 
      functional pancreatic beta cells from diabetic patient-derived stem cells to 
      replace the dysfunctional cells, thereby compensating for insulin deficiency and 
      reducing the comorbidities of the disease and its associated financial and social 
      burden on the patient and society. Beta-like cells generated by most current 
      differentiation protocols have blunted functionality compared to their adult 
      human counterparts. The Ca(2+) dynamics in stem cell-derived beta-like cells and 
      adult beta cells are summarized in this review, revealing the importance of 
      proper Ca(2+) homeostasis in beta-cell function. Consequently, the importance of 
      targeting Ca(2+) function in differentiation protocols is suggested to improve 
      current strategies to use hPSCs to generate mature and functional beta-like cells 
      with a comparable glucose-stimulated insulin secretion (GSIS) profile to adult 
      beta cells.
FAU - Mu-U-Min, Razik Bin Abdul
AU  - Mu-U-Min RBA
AD  - Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin 
      Khalifa University (HBKU), Qatar Foundation (QF), Doha P.O. Box 34110, Qatar.
FAU - Diane, Abdoulaye
AU  - Diane A
AD  - Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin 
      Khalifa University (HBKU), Qatar Foundation (QF), Doha P.O. Box 34110, Qatar.
FAU - Allouch, Asma
AU  - Allouch A
AD  - Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin 
      Khalifa University (HBKU), Qatar Foundation (QF), Doha P.O. Box 34110, Qatar.
FAU - Al-Siddiqi, Heba H
AU  - Al-Siddiqi HH
AD  - Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin 
      Khalifa University (HBKU), Qatar Foundation (QF), Doha P.O. Box 34110, Qatar.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230529
PL  - Switzerland
TA  - Biomedicines
JT  - Biomedicines
JID - 101691304
PMC - PMC10296018
OTO - NOTNLM
OT  - beta cells
OT  - calcium signaling
OT  - diabetes
OT  - differentiation
OT  - stem cells
COIS- The authors declare no conflict of interest.
EDAT- 2023/06/28 06:42
MHDA- 2023/06/28 06:43
PMCR- 2023/05/29
CRDT- 2023/06/28 01:08
PHST- 2023/04/17 00:00 [received]
PHST- 2023/05/18 00:00 [revised]
PHST- 2023/05/23 00:00 [accepted]
PHST- 2023/06/28 06:43 [medline]
PHST- 2023/06/28 06:42 [pubmed]
PHST- 2023/06/28 01:08 [entrez]
PHST- 2023/05/29 00:00 [pmc-release]
AID - biomedicines11061577 [pii]
AID - biomedicines-11-01577 [pii]
AID - 10.3390/biomedicines11061577 [doi]
PST - epublish
SO  - Biomedicines. 2023 May 29;11(6):1577. doi: 10.3390/biomedicines11061577.