ReviewCell communication and signaling : CCS2025
The hidden driver of osteoporosis: mitochondria-dominated inflammation.
Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Small but mighty: mitochondrial DNA at the centre of retrograde signalling.Cell communication and signaling : CCS · 2026Review
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
Abstract
Mitochondria are powerful multifunctional intracellular organelles involved in a wide array of cellular processes. Emerging evidence has highlighted mitochondria as pivotal activators of innate immunity and key participants in inflammatory responses, including in sterile inflammatory diseases, beyond their well-established role as the "powerhouse" of cells. Osteoporosis (OP) is a metabolic disorder characterized by chronic low-grade inflammation, suggesting potential therapeutic value for OP treatment by targeting mitochondria-driven inflammatory pathways. Current research on mitochondrial involvement in OP primarily focuses on its functions in energy metabolism, calcium signaling transduction, oxidative stress, and cell death. However, it remains elusive regarding the precise relationship between mitochondria-mediated inflammatory mechanisms and OP pathogenesis. Accordingly, this review aims to synthesize recent advancement in understanding mitochondria-mediated inflammatory mechanisms and their implications in OP development, to offer insights that may inform future mechanistic investigations and therapeutic strategy development.
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.