SynthesisPurinergic signalling2026
Interaction between purinergic signalling and purinergic modulators with skin wound repair effectors: a systematic review of preclinical in vivo models.
Synthesis in Purinergic signalling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purinergic signalling plays a central regulatory role on cell proliferation, migration, differentiation, survival, and inflammation. However, the impact of purinergic modulators-based therapies on tissue repair is still overlooked. By using a systematic review framework, we investigated the therapeutic relevance of purinergic agonists and antagonists in animal models of skin wound healing. Following PRISMA guidelines, PubMed/Medline, Scopus, Web of Science, Embase, and CINAHL databases were searched, identifying 12 in vivo preclinical studies. Risk of bias was assessed using the SYRCLE tool. Topical or oral administration of CGS-21680 (4-[{N-ethyl-5'-carbamoyladenos-2-yl}aminoethyl] phenylpropionic acid), UTP (Uridine-5'-triphosphate), NECA (5'-N-ethylcarboxamidoadenosine), ATP (adenosine triphosphate), PDRN (polydeoxyribonucleotide), ADP (Adenosine-5'-diphosphate) and TMPS (Thymidine 5'-O-monophosphorothioate) agonists stimulated wound contraction, fibroblast and keratinocyte proliferation, angiogenesis, and collagen biosynthesis. These effects were associated with activation of Nrf2 (Nuclear factor erythroid 2-related factor 2), MAPK (Mitogen-Activated Protein Kinase), and ERK/CREB pathways, inflammation and oxidative/nitrosative stress down-regulation, and increased anti-inflammatory/regulatory cytokines (IL-10, IL-13, TGF-β) and growth factors (FGF, EGF). Conversely, the purinergic antagonists DMPX (3,7-dimethyl-1-propargylxanthine), CSC (8-(3-chlorostyryl) caffeine), SUR (Suramin), ENP (enprofylline), caffeine, CLOP (clopidogrel), MRS 2179 (2'-deoxy-N6-methyladenosine-3',5'-bisphosphate), and MRS 2395 (2-Chloro-3',5'-O-(benzoyl-β,γ-methylene) adenosine 5'-triphosphate), as well as genetic knockout for purinergic receptors delayed wound closure by inhibiting these pathways, impairing angiogenesis, collagenogenesis, and aggravating inflammation and oxidative damage. Purinergic agonists were associated with improved wound healing through inflammatory and oxidative modulation, enhanced angiogenesis, increased cell proliferation, and accelerated wound closure, whereas antagonists or genetic deficiency of purinergic receptors impaired tissue repair. This review was registered in the PROSPERO database (CRD420251010254).
Indexed as
Identifiers
What Socratic holds
Registered trials
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.