ReviewAmerican journal of physiology. Cell physiology2020
Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.
Review in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 55 citations in OpenAlex.
- Exercise-specific epigenetic effects on cardiovascular health.Clinical epigenetics · 2026Review
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Age and Sex Impact the Role of Thrombospondin-2 and Thrombospondin-5 in Response to Hindlimb Ischemia.FASEB bioAdvances · 2026Article
- Review
- THBS1 regulates the function and insulin sensitivity of HTR8/SVneo cells treated with high glucose through the RhoA/ROCK1 signaling pathway.Diabetology & metabolic syndrome · 2025Article
- Long-term exercise enhances meningeal lymphatic vessel plasticity and drainage in a mouse model of Alzheimer's disease.Translational neurodegeneration · 2025Article
- Targeting Aging Hallmarks with Monoclonal Antibodies: A New Era in Cancer Immunotherapy and Geriatric Medicine.International journal of molecular sciences · 2025Review
- The Proteome Content of Blood Clots Observed Under Different Conditions: Successful Role in Predicting Clot Amyloid(ogenicity).Molecules (Basel, Switzerland) · 2025Review
- Suppression of thrombospondin-1-mediated inflammaging prolongs hematopoietic health span.Science immunology · 2025Article
- Transcriptomic predictors of rapid progression from mild cognitive impairment to Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Thrombospondin-1 mitigates osteoarthritis progression by inhibiting mechanical stress-induced chondrocyte ferroptosis via the integrin/YAP pathway.Frontiers in immunology · 2025Article
- Recent Developments in Glioblastoma-On-A-Chip for Advanced Drug Screening Applications.Small (Weinheim an der Bergstrasse, Germany) · 2025Review
- Matrix-free human lung organoids derived from induced pluripotent stem cells to model lung injury.Stem cell research & therapy · 2024Article
- Thrombospondin-1 promotes fibro-adipogenic stromal expansion and contractile dysfunction of the diaphragm in obesity.JCI insight · 2024Article
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- Effect of cellular senescence on the response of human peritoneal mesothelial cells to TGF-β.Scientific reports · 2024Article
- Positive and negative feedback regulation of the TGF-β1 explains two equilibrium states in skin aging.iScience · 2024Article
- Emerging functions of thrombospondin-1 in immunity.Seminars in cell & developmental biology · 2024Review
- Nervonic Acid Inhibits Replicative Senescence of Human Wharton's Jelly-Derived Mesenchymal Stem Cells.International journal of stem cells · 2024Article
- Tolerating CD47.Clinical and translational medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Numerous age-dependent alterations at the molecular, cellular, tissue and organ systems levels underlie the pathophysiology of aging. Herein, the focus is upon the secreted protein thrombospondin-1 (TSP1) as a promoter of aging and age-related diseases. TSP1 has several physiological functions in youth, including promoting neural synapse formation, mediating responses to ischemic and genotoxic stress, minimizing hemorrhage, limiting angiogenesis, and supporting wound healing. These acute functions of TSP1 generally require only transient expression of the protein. However, accumulating basic and clinical data reinforce the view that chronic diseases of aging are associated with accumulation of TSP1 in the extracellular matrix, which is a significant maladaptive contributor to the aging process. Identification of the relevant cell types that chronically produce and respond to TSP1 and the molecular mechanisms that mediate the resulting maladaptive responses could direct the development of therapeutic agents to delay or revert age-associated maladies.
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.