ArticleNPJ aging and mechanisms of disease2021
A decrease in NAD
Article in NPJ aging and mechanisms of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 55 citations in OpenAlex.
- Baseline serum metabolites predict fractures in individuals who were Black and had type 2 diabetes.Frontiers in endocrinology · 2026Trial
- A sustained NADBioactive materials · 2026Article
- Inducible chronic NAD deficiency in mice reveals multi-systemic phenotypical, metabolic, and transcriptional changes.Nature communications · 2026Article
- Bone Aging and Glycative Stress: Convergent and Divergent Mechanisms Driving Skeletal Deterioration.Cells · 2026Review
- Autophagy in Osx1-Cre-targeted cells is essential for development, growth, and maintenance of bone.Bone reports · 2026Article
- Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026Review
- Review
- Effects of low-level laser therapy on the aging process of human dermal fibroblast cells.Lasers in medical science · 2026Article
- Article
- The triangular drivers of bone aging: mechanistic insights and therapeutic targets in cellular senescence, estrogen deficiency, and gut microenvironment dysregulation.Frontiers in cell and developmental biology · 2026Review
- Article
- Article
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Epigenetic Regulation of Bone Healing: Implications for Fracture Repair and Clinical Treatment Strategies.The Yale journal of biology and medicine · 2025Review
- Article
- Biomechanical Basis for Bone Healing and Osseointegration of Implants in Sinus Grafts.Clinical implant dentistry and related research · 2025Review
- Restoring bone healing potential.eLife · 2025Article
- Macrophages in osteoporotic fractures: from immunometabolic mechanisms to precision therapeutic approaches.Frontiers in endocrinology · 2025Review
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Age-related osteoporosis is caused by a deficit in osteoblasts, the cells that secrete bone matrix. The number of osteoblast progenitors also declines with age associated with increased markers of cell senescence. The forkhead box O (FoxO) transcription factors attenuate Wnt/β-catenin signaling and the proliferation of osteoprogenitors, thereby decreasing bone formation. The NAD
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.