Evidence map›Paper›PMID 39203802›Full record

ArticleNutrients2024

Nicotinamide Suppresses Hyperactivation of Dendritic Cells to Control Autoimmune Disease through PARP Dependent Signaling.

Ai-Ping Cao, Yun-Ying Wang, Yan-Yan Shen, Yan-Hong Liu, Jia-Yu Liu, Yao Wang, Yue Guo, Rui-Bo Wang, Bo-Yang Xie, Xin Pan and 4 more

Abstract read
In one paragraph

Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. 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

14 authors.

Ai-Ping CaoInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310016, China.
Yun-Ying WangNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Yan-Yan ShenNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Yan-Hong LiuNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Jia-Yu LiuNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Yao WangNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Yue GuoNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Rui-Bo WangNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Bo-Yang XieNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Xin PanNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.ORCID 0000-0002-1982-2261
Ai-Ling LiInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310016, China.
Qing XiaNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Wei-Na ZhangNanhu Laboratory, National Center of Biomedical Analysis, Beijing 100039, China.
Tao ZhouInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310016, China.ORCID 0000-0001-6222-2053

Funding

Nanhu Laboratory NSS2024CI05004National Natural Science Foundation of China 82022030National Natural Science Foundation of China 82273024
6 · The paper itself

Abstract

Dendritic cells (DCs) are crucial in initiating and shaping both innate and adaptive immune responses. Clinical studies and experimental models have highlighted their significant involvement in various autoimmune diseases, positioning them as promising therapeutic targets. Nicotinamide (NAM), a form of vitamin B3, with its anti-inflammatory properties, has been suggested, while the involvement of NAM in DCs regulation remains elusive. Here, through analyzing publicly available databases, we observe substantial alterations in NAM levels and NAM metabolic pathways during DCs activation. Furthermore, we discover that NAM, but not Nicotinamide Mononucleotide (NMN), significantly inhibits DCs over-activation in vitro and in vivo. The suppression of DCs hyperactivation effectively alleviates symptoms of psoriasis. Mechanistically, NAM impairs DCs activation through a Poly (ADP-ribose) polymerases (PARPs)-NF-κB dependent manner. Notably, phosphoribosyl transferase (NAMPT) and PARPs are significantly upregulated in lipopolysaccharide (LPS)-stimulated DCs and psoriasis patients; elevated NAMPT and PARPs expression in psoriasis patients correlates with higher psoriasis area and severity index (PASI) scores. In summary, our findings underscore the pivotal role of NAM in modulating DCs functions and autoimmune disorders. Targeting the NAMPT-PARP axis emerges as a promising therapeutic approach for DC-related diseases.

Indexed as

Autoimmune DiseasesDendritic CellsNiacinamideNicotinamide PhosphoribosyltransferasePoly(ADP-ribose) PolymerasesPsoriasisSignal TransductionAnimalsHumansLipopolysaccharidesMiceMice, Inbred C57BLNF-kappa BLipopolysaccharidesNF-kappa BNiacinamideNicotinamide PhosphoribosyltransferasePoly(ADP-ribose) Polymerasesdendritic cellNF-κBnicotinamidePARPpsoriasis

Identifiers

PMID39203802
PMCPMC11356829

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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.