ArticleMolecular biology reports2022
Substance P modulates BMSCs migration for tissue repair through NK-1R/CXCR4/p-Akt signal activation.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment.Journal of orthopaedic translation · 2026Review
- Effects of fatty acids and cholesterol on functions and behavior of bone marrow mesenchymal stem cells.iScience · 2026Review
- Neuro-immune-vascular-stem cell crosstalk in bone/cartilage regeneration: mechanisms, technological advances, and clinical perspectives.Frontiers in bioengineering and biotechnology · 2026Review
- Neuro-immune-bone axis in post-traumatic bone regeneration: temporal regulation, dysregulation mechanisms, and therapeutic implications.Frontiers in immunology · 2026Review
- Decoding Pain: Next-Generation In Vitro Systems for Mechanistic Insights and Drug Discovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- The ratio of alpha-calcitonin gene-related peptide to substance P is associated with the transition of bone metabolic states during aging and healing.Journal of molecular histology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe migration of bone marrow-derived mesenchymal stem cells (BMSCs) to the wound site played an important role in tissue repair. Substance P (SP) has been studied and reported to be involved in tissue repair by promoting the growth of endothelial cells and the migration of BMSCs. However, the complicated process and the molecular mechanisms were not fully understood. Thus, we aimed to investigate the effect of SP-induced BMSCs migration on tissue repair and its possible mechanism. METHODS AND
resultsWestern blot and q-PCR assay revealed that SP could induce the BMSCs migration through overexpression of CXCR4 and upregulation of Akt phosphorylation. And the upregulation was related to the activation of neurokinin-1 receptor (NK-1R). Besides, we found that the increased phosphorylation Akt caused by SP could be canceled by the inhibition of CXCR4 both in vitro and in vivo. Furthermore, a skin-injury animal model was established and used to observe the tissue repair process. Results showed that SP could accelerate wound closure, gain more granulation tissue accumulation, and more collagen deposition through the promotion of angiogenesis and induction of the BMSCs migration to the wound site. And these effects could be impaired by inhibition of CXCR4 and p-Akt.
conclusionsOur results suggested that SP promoted tissue repair through BMSCs migration via upregulation of CXCR4 and p-Akt. The expression of CXCR4 and p-Akt were regulated by NK-1R activation. These findings add more evidence in understanding the mechanisms of SP-induced BMSCs migration and highlight the potential for clinical implementation of SP in tissue repair.
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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 OpenQuestion graph.