ArticleBone research2025
Injured bone-triggered osteokines secretion promotes diabetic wound healing.
Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Bone‑origin repair in diabetic foot ulcers: Mechanisms of callus formation and endocrine effects in healing (Review).International journal of molecular medicine · 2026Review
- Alginate-Chitosan Gel Microbeads for PhiKZ Encapsulation as a Model of Bacteriophage Delivery to CombatGels (Basel, Switzerland) · 2026Article
- Unlocking bone repair in osteoporosis by targeting the angiogenic niche.Frontiers in endocrinology · 2026Review
- Targeting persistently activated inflammatory microenvironment to promote chronic wound healing.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The treatment of severe diabetic foot remains a clinical challenge. While it is established that bone can exert systemic effects through the secretion of osteokines on other organs, whether this endocrine function can be harnessed to promote diabetic wound healing remains unexplored. Here, we investigate the impact of a bone injury strategy on diabetic wound healing, leveraging the body's innate regenerative capacity to stimulate osteokine release and influence remote skin wound repair. This study demonstrates that the tibial defect significantly accelerates ipsilateral diabetic foot skin wound healing. Mechanistically, we identify osteokines, platelet-derived growth factor-BB (PDGF-BB), as the key to initiating this process. Bone defect triggers a substantial release of PDGF-BB, which reaches the skin wound site via peripheral circulation. At the skin wound site, PDGF-BB mediates the secretion of keratinocyte growth factor (KGF) from fibroblasts via the PDGFRβ signaling pathway, thereby promoting the rapid re-epithelialization of epidermal cells through a paracrine pathway. Additionally, elevated PDGF-BB levels enhance the regeneration of CD31
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.