Evidence map›Paper›PMID 36747753›Full record

ArticlebioRxiv : the preprint server for biology2024

Skin keratinocyte-derived SIRT1 and BDNF modulate mechanical allodynia in mouse models of diabetic neuropathy.

Jennifer O'Brien, Peter Niehaus, Koping Chang, Juliana Remark, Joy Barrett, Abhishikta Dasgupta, Morayo Adenegan, Mohammad Salimian, Yanni Kevas, Krish Chandrasekaran and 7 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 5 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 2 countries.

Jennifer O'BrienDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Peter NiehausDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Koping ChangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Juliana RemarkHansj rg Wyss Department of Plastic Surgery, Department of Cell Biology, New York University School of Medicine, New York, NY, 10016, USA.
Joy BarrettHansj rg Wyss Department of Plastic Surgery, Department of Cell Biology, New York University School of Medicine, New York, NY, 10016, USA.
Abhishikta DasguptaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Morayo AdeneganDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Mohammad SalimianDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Yanni KevasDepartment of Neurology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Krish ChandrasekaranDepartment of Neurology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Tibor KristianBaltimore Veterans Affairs Medical Center, Baltimore, MD, 21201, USA.
Rajeshwari ChellappanDepartment of Pathology, University of Alabama Birmingham, Birmingham, AL, 35233, USA.
Samuel RubinDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Ashley KiemenDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Catherine Pei-Ju LuHansj rg Wyss Department of Plastic Surgery, Department of Cell Biology, New York University School of Medicine, New York, NY, 10016, USA.
James W RussellDepartment of Neurology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Cheng-Ying HoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.ORCID 0000-0002-9866-8572
University of Maryland, Baltimore · USJohns Hopkins University · USNew York University · USUniversity of Alabama at Birmingham · US

Funding

NAD+ and SIRT1 Regulate Mitochondrial Function in Diabetic NeuropathyR01DK107007 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI RUSSELL, JAMES W · 2016 to 2021
$2.3M
Using NAD+ precursor for treatment of global cerebral ischemiaR01NS119275 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI KRISTIAN, TIBOR · 2021 to 2025
$1.9M
The role of skin BDNF in the maintenance of the cutaneous mechanosensory nervous systemK08NS102468 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI HO, CHENG-YING · 2018 to 2022
$1.0M
Understanding the Molecular Mechanisms of Neuronal Control in Sweat Gland DevelopmentF30HD105455 · NICHD · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI REMARK, JULIANA THERESA · 2021 to 2024
$151k
The role of nicotinamide mononucleotide dependent mitochondrial reactive oxygen species generation in acute brain injuryI01BX004895 · VA · BALTIMORE VA MEDICAL CENTER · PI KRISTIAN, TIBOR · 2020 to 2024
–
BLRD VA I01 BX004895NICHD NIH HHS F30 HD105455NIDDK NIH HHS R01 DK107007NINDS NIH HHS K08 NS102468NINDS NIH HHS R01 NS119275
6 · The paper itself

Abstract

Diabetic neuropathy is a debilitating disorder characterized by spontaneous and mechanical pain. The role of skin mechanoreceptors in the development of mechanical pain (allodynia) is unclear. We discovered that mice with diabetic neuropathy had decreased sirtuin 1 (SIRT1) deacetylase activity in foot skin, leading to reduced expression of brain-derived neurotrophic factor (BDNF) and subsequent loss of innervation in Meissner corpuscles, a mechanoreceptor expressing the BDNF receptor TrkB. When SIRT1 was depleted from skin, the mechanical allodynia worsened in diabetic neuropathy mice, likely due to retrograde degeneration of the Meissner-corpuscle innervating Aβ axons and aberrant formation of Meissner corpuscles which may have increased the mechanosensitivity. The same phenomenon was also noted in skin BDNF knockout mice. Furthermore, overexpression of SIRT1 in skin induced Meissner corpuscle reinnervation and regeneration, resulting in significant improvement of diabetic mechanical allodynia. Overall, the findings suggested that skin-derived SIRT1 and BDNF function in the same pathway in skin sensory apparatus regeneration and highlighted the potential of developing topical SIRT1-activating compounds as a novel treatment for diabetic mechanical allodynia.

Indexed as

BDNFDiabetic neuropathymechanical allodyniaSIRT1skin

Identifiers

PMID36747753
PMCPMC9900813
OpenAlexW4318037171

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.