ReviewCalcified tissue international2026
SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.
Review in Calcified tissue international, 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
4 authors.
Funding
Abstract
SERPINE1 encodes plasminogen activator inhibitor-1 (PAI-1), a key inhibitor of tissue-type and urokinase-type plasminogen activators. Beyond fibrinolysis, PAI-1 participates in extracellular matrix remodeling, cellular senescence, inflammatory amplification, fibrosis-like repair, metabolic stress responses, and bone-cell coupling. These processes are central to osteoporosis, osteoarthritis, and intervertebral disc degeneration, yet the role of SERPINE1/PAI-1 in skeletal tissues is highly context dependent. In osteoporosis, excessive PAI-1 activity is mainly associated with impaired osteogenesis, osteoblast-lineage senescence, defective repair, and bone loss. In osteoarthritis, PAI-1 shows a context-dependent role: persistent elevation may promote chondrocyte senescence and maladaptive matrix remodeling, whereas experimental loss-of-function studies suggest that PAI-1 may protect cartilage in specific settings by restraining excessive plasmin-MMP-mediated degradation. In intervertebral disc degeneration, emerging evidence links SERPINE1 expression and PAI-1 activity to nucleus pulposus cell senescence, fibrosis-like extracellular matrix remodeling, oxidative/metabolic stress, and matrix dysregulation. This review synthesizes current evidence and proposes a testable conceptual framework in which SERPINE1/PAI-1 may function as a stress-responsive remodeling rheostat rather than as a uniformly pathogenic or protective factor. From a translational perspective, SERPINE1/PAI-1 is unlikely to serve as a stand-alone diagnostic biomarker or a target for uniform systemic inhibition. Instead, its clinical value may lie in molecular stratification, identification of disease-stage- and compartment-specific endotypes, and locally targeted modulation of pathogenic downstream programs. Future studies should integrate spatial multi-omics, time-resolved disease models, human cohort validation, and tissue-specific delivery strategies to determine when SERPINE1/PAI-1 is therapeutically actionable in skeletal degeneration.
Indexed as
Identifiers
42726129What 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.