Evidence map›Paper›PMID 32119761›Full record

ArticleJournal of cellular and molecular medicine2020

SIRT3 deficiency delays diabetic skin wound healing via oxidative stress and necroptosis enhancement.

Shengju Yang, Mengting Xu, Guoliang Meng, Yan Lu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  11. SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis.Frontiers in cell and developmental biology · 2025
    Review
  12. Apoptosis and Cell Clearance in Skin Wound Healing.Advances in experimental medicine and biology · 2025
    Review
  13. Review
  14. Article
  15. Bioengineered MSCCellular and molecular life sciences : CMLS · 2024
    Article
  16. Review
  17. Article
  18. Article
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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

4 authors at 2 institutions in 1 country.

Shengju YangDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mengting XuDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong, China.
Guoliang MengDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong, China.
Yan LuDepartment of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0003-3358-4164
Nantong University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sirtuin 3 (SIRT3) plays a vital role in several dermatological diseases. However, the role and detailed mechanism of SIRT3 in diabetic wound healing are unknown well yet. To explore possible involvement of SIRT3 and necroptosis in diabetic skin wound healing, SIRT3 knockout (KO) mice and 129S1/SvImJ wild-type (WT) mice were injected with streptozotocin (STZ), and mice skin fibroblasts were exposed to high glucose (HG). It was found that SIRT3 expression decreased in the skin of diabetic patients. SIRT3 deficiency delayed healing rate, reduced blood supply and vascular endothelial growth factor expression, promoted superoxide production, increased malondialdehyde (MDA) levels, decreased total antioxidant capacity (T-AOC), reduced superoxide dismutase (SOD) activity and aggravated ultrastructure disorder in skin wound of diabetic mice. SIRT3 deficiency inhibited mice skin fibroblasts migration with HG stimulation, which was restored by SIRT3 overexpression. SIRT3 deficiency also suppressed α-smooth muscle actin (α-SMA) expression, enhanced superoxide production but decreased mitochondrial membrane potential with HG stimulation after scratch. SIRT3 deficiency further elevated receptor-interacting protein kinase 3 (RIPK3), RIPK1 and caspase 3 expression both in vitro and in vivo. Collectively, SIRT3 deficiency delayed skin wound healing in diabetes, the mechanism might be related to impaired mitochondria function, enhanced oxidative stress and increased necroptosis. This may provide a novel therapeutic target to accelerate diabetic skin wound healing.

Indexed as

AnimalsCaspase 3Diabetes Mellitus, ExperimentalGlucoseHumansMiceMice, Inbred NODMice, KnockoutNecroptosisOxidative StressReceptor-Interacting Protein Serine-Threonine KinasesSirtuin 3SkinWound HealingCaspase 3GlucoseReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouseRipk3 protein, mouseSirt3 protein, mouseSirtuin 3diabetes mellitusnecroptosisoxidative stressSirtuin 3skin fibroblastsskin wound healing

Identifiers

PMID32119761
PMCPMC7176871
OpenAlexW3009728012

What OpenQuestion holds

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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.