Evidence map›Paper›PMID 40948991›Full record

ReviewJournal of experimental pharmacology2025

Diabetic Peripheral Neuropathy: Pathophysiology and New Insights into the Mechanism of Action of High-Concentration Topical Capsaicin.

David G Armstrong, Keith Bley, David M Simpson, Peter Staats, Samuel Allen, Audrey Carnevale, Lizandra Marcondes

Abstract readReview
In one paragraph

Review in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. 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

7 authors.

David G ArmstrongKeck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0003-1887-9175
Keith BleyPyrotech Therapeutics, Inc., Beijing, People's Republic of China.
David M SimpsonDepartment of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Peter StaatsVagus Nerve Society, Atlantic Beach, FL, USA.ORCID 0000-0002-4079-5165
Samuel AllenAveritas Pharma, Inc., Morristown, NJ, USA.ORCID 0009-0000-0916-0199
Audrey CarnevaleAveritas Pharma, Inc., Morristown, NJ, USA.ORCID 0009-0003-6036-9707
Lizandra MarcondesAveritas Pharma, Inc., Morristown, NJ, USA.ORCID 0009-0001-3091-0924

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic peripheral neuropathy (DPN) is a chronic, progressive complication of diabetes. Pain in DPN can be severe and detrimental to the patient's quality of life. In this review, we provide an update on the mechanism of action (MOA) of high-concentration capsaicin topical system (HCCTS) for treatment of painful DPN, with an emphasis on neuroregeneration. In diabetes, hyperglycemia and other metabolic imbalances lead to oxidative stress and inflammation, which result in degeneration of the axons of afferent neurons (particularly C and Aδ fibers) within the peripheral nervous system. Dysfunction of the microvasculature supporting the nerves further exacerbates neural damage. As a result, epidermal nerve fiber density (ENFD) diminishes, and physical and chemical changes to the remaining afferent fibers render them hypersensitive to painful stimuli and hyposensitive to normal stimuli. As the longest axons are usually damaged first, DPN normally begins in the feet, then legs, and finally the hands. HCCTS incorporates a matrix technology that forcibly diffuses a high concentration of capsaicin (a TRPV1 agonist) to the dermis and epidermis, targeting TRPV1 receptors that are upregulated in DPN and play a key role in pain generation. HCCTS activates TRPV1 receptors expressed on the neuron cell membrane and endoplasmic reticulum, leading to cytoplasmic calcium ion overload, and then a cascade of cellular events resulting in reversible neurolysis of these afferent terminals. After 1-3 months, the terminals regenerate with a "healthier" phenotype, increasing ENFD, resulting in vasodilation, which may lead to a microenvironment conducive to improved neuroregeneration. This MOA is supported by clinical evidence demonstrating that repeated HCCTS treatment provides cumulative benefits in pain and improvements in sensory function of the feet compared with baseline. If effects on sensory function are confirmed in large-scale clinical studies, HCCTS could help slow the progression of DPN to more severe forms of diabetic foot syndrome.

Indexed as

capsaicindegenerationDPNhyperalgesianeurolysisTRPV1

Identifiers

PMID40948991
PMCPMC12433221

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Registered trials

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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.