PMID- 32216738
OWN - NLM
STAT- MEDLINE
DCOM- 20210929
LR  - 20231112
IS  - 1875-5739 (Electronic)
IS  - 1567-2026 (Print)
IS  - 1567-2026 (Linking)
VI  - 17
IP  - 3
DP  - 2020
TI  - Prospects and Perspectives for WISP1 (CCN4) in Diabetes Mellitus.
PG  - 327-331
LID - 10.2174/1567202617666200327125257 [doi]
AB  - The prevalence of diabetes mellitus (DM) continues to increase throughout the 
      world. In the United States (US) alone, approximately ten percent of the 
      population is diagnosed with DM and another thirty-five percent of the population 
      is considered to have prediabetes. Yet, current treatments for DM are limited and 
      can fail to block the progression of multi-organ failure over time. Wnt1 
      inducible signaling pathway protein 1 (WISP1), also known as CCN4, is a 
      matricellular protein that offers exceptional promise to address underlying 
      disease progression and develop innovative therapies for DM. WISP1 holds an 
      intricate relationship with other primary pathways of metabolism that include 
      protein kinase B (Akt), mechanistic target of rapamycin (mTOR), AMP activated 
      protein kinase (AMPK), silent mating type information regulation 2 homolog 1 
      (Saccharomyces cerevisiae) (SIRT1), and mammalian forkhead transcription factors 
      (FoxOs). WISP1 is an exciting prospect to foster vascular as well as neuronal 
      cellular protection and regeneration, control cellular senescence, block 
      oxidative stress injury, and maintain glucose homeostasis. However, under some 
      scenarios WISP1 can promote tumorigenesis, lead to obesity progression with 
      adipocyte hyperplasia, foster fibrotic hepatic disease, and lead to dysregulated 
      inflammation with the progression of DM. Given these considerations, it is 
      imperative to further elucidate the complex relationship WISP1 holds with other 
      vital metabolic pathways to successfully develop WISP1 as a clinically effective 
      target for DM and metabolic disorders.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Maiese, Kenneth
AU  - Maiese K
AD  - Cellular and Molecular Signaling, New York, NY 10022, United States.
LA  - eng
GR  - R01 NS053946/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Neurovasc Res
JT  - Current neurovascular research
JID - 101208439
RN  - 0 (CCN Intercellular Signaling Proteins)
RN  - 0 (CCN4 protein, human)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Animals
MH  - CCN Intercellular Signaling Proteins/*metabolism/pharmacology/*therapeutic use
MH  - Diabetes Mellitus/*drug therapy/*metabolism
MH  - Humans
MH  - Hypoglycemic Agents/metabolism/pharmacology/therapeutic use
MH  - Metabolic Networks and Pathways/*drug effects/physiology
MH  - Proto-Oncogene Proteins/*metabolism/pharmacology/*therapeutic use
PMC - PMC7529678
MID - NIHMS1580037
OTO - NOTNLM
OT  - AMP activated protein kinase (AMPK)
OT  - Akt
OT  - CCN4
OT  - FoxO
OT  - WISP-1
OT  - Wnt
OT  - Wnt1 inducible signaling pathway protein 1 (WISP1)
OT  - autophagy
OT  - cancer
OT  - diabetes mellitus
OT  - forkhead transcription factors
OT  - inflammation
OT  - interleukin 18 (IL-18)
OT  - mechanistic target of rapamycin (mTOR)
OT  - oxidative stress
OT  - silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) 
      (SIRT1)
OT  - sirtuin
OT  - stem cells
OT  - wingless
EDAT- 2020/03/29 06:00
MHDA- 2021/09/30 06:00
PMCR- 2020/10/08
CRDT- 2020/03/29 06:00
PHST- 2020/02/28 00:00 [received]
PHST- 2020/03/10 00:00 [revised]
PHST- 2020/03/16 00:00 [accepted]
PHST- 2020/03/29 06:00 [pubmed]
PHST- 2021/09/30 06:00 [medline]
PHST- 2020/03/29 06:00 [entrez]
PHST- 2020/10/08 00:00 [pmc-release]
AID - CNR-EPUB-105500 [pii]
AID - CNR-17-327 [pii]
AID - 10.2174/1567202617666200327125257 [doi]
PST - ppublish
SO  - Curr Neurovasc Res. 2020;17(3):327-331. doi: 10.2174/1567202617666200327125257.