Evidence map›Paper›PMID 28338622›Full record

ReviewInternational journal of molecular sciences2017

Phosphodiesterase Inhibitors as a Therapeutic Approach to Neuroprotection and Repair.

Eric P Knott, Mazen Assi, Sudheendra N R Rao, Mousumi Ghosh, Damien D Pearse

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. In the Brain of Phosphodiesterases: Potential Therapeutic Targets for Schizophrenia.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. PDE2A Inhibition Enhances Axonal Sprouting, Functional Connectivity, and Recovery after Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Research progress of phosphodiesterase inhibitors in inflammatory bowel disease treatment.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  17. Review
  18. Article
  19. The Potent PDE10A Inhibitor MP-10 (PF-2545920) Suppresses Microglial Activation in LPS-Induced Neuroinflammation and MPTP-Induced Parkinson's Disease Mouse Models.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Eric P KnottHerbert Wertheim College of Medicine, Florida International University, Miami, FL 33199, USA. eknott@emory.edu.
Mazen AssiThe Miami Project to Cure Paralysis, The Miller School of Medicine at the University of Miami, Miami, FL 33136, USA. m_assi2010@live.com.
Sudheendra N R RaoThe Miami Project to Cure Paralysis, The Miller School of Medicine at the University of Miami, Miami, FL 33136, USA. sudhee26@med.miami.edu.
Mousumi GhoshThe Miami Project to Cure Paralysis, The Miller School of Medicine at the University of Miami, Miami, FL 33136, USA. mghosh@med.miami.edu.
Damien D PearseThe Miami Project to Cure Paralysis, The Miller School of Medicine at the University of Miami, Miami, FL 33136, USA. DPearse@med.miami.edu.
University of Miami · USFlorida International University · USNeurological Surgery · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A wide diversity of perturbations of the central nervous system (CNS) result in structural damage to the neuroarchitecture and cellular defects, which in turn are accompanied by neurological dysfunction and abortive endogenous neurorepair. Altering intracellular signaling pathways involved in inflammation and immune regulation, neural cell death, axon plasticity and remyelination has shown therapeutic benefit in experimental models of neurological disease and trauma. The second messengers, cyclic adenosine monophosphate (cyclic AMP) and cyclic guanosine monophosphate (cyclic GMP), are two such intracellular signaling targets, the elevation of which has produced beneficial cellular effects within a range of CNS pathologies. The only known negative regulators of cyclic nucleotides are a family of enzymes called phosphodiesterases (PDEs) that hydrolyze cyclic nucleotides into adenosine monophosphate (AMP) or guanylate monophosphate (GMP). Herein, we discuss the structure and physiological function as well as the roles PDEs play in pathological processes of the diseased or injured CNS. Further we review the approaches that have been employed therapeutically in experimental paradigms to block PDE expression or activity and in turn elevate cyclic nucleotide levels to mediate neuroprotection or neurorepair as well as discuss both the translational pathway and current limitations in moving new PDE-targeted therapies to the clinic.

Indexed as

AnimalsCentral Nervous SystemCentral Nervous System DiseasesCyclic AMPCyclic GMPHumansPhosphodiesterase InhibitorsPhosphoric Diester HydrolasesRegenerationSecond Messenger SystemsSignal TransductionCyclic AMPCyclic GMPPhosphodiesterase InhibitorsPhosphoric Diester Hydrolasescell deathclinical trialsCNScyclic AMPcyclic GMPcyclic nucleotidesPDEphosphodiesterasephosphodiesterase inhibitorregenerationrepair

Identifiers

PMID28338622
PMCPMC5412282
OpenAlexW2600321935

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.