ArticleJCI insight2023
Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 34 citations in OpenAlex.
- Senescent obesity signature in breast cancer: a paradigm of reverse cardio-oncology.European heart journal · 2026Review
- Natural Killer Cell Dysfunction Is Emerging During Midlife Obesity.Aging cell · 2026Article
- Solute Carrier Family 1 Member 5 (SLC1A5)-dependent glutamine transport regulates macrophage senescence and efferocytosis during liver regeneration.Molecular biomedicine · 2026Article
- The ageing immune system as a driver of systemic ageing.Nature reviews. Immunology · 2026Review
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Visceral adiposity, metabolic health and aging.Nature aging · 2026Review
- Adipocytes as core drivers of skin aging and novel targets for regeneration.Biogerontology · 2026Review
- Ligature-induced periodontitis in mice potentially accelerates CD4Frontiers in immunology · 2026Article
- Mechano-immune interactions in musculoskeletal aging: Mechanisms and translational perspectives.Theranostics · 2026Review
- The fat-heart entanglement and the role of 'osteopontin mechanics' in cardiometabolic senescence.European journal of clinical investigation · 2026Review
- Adipose immune microenvironment: catalyst of age-related adipose tissue dysfunction.Immunity & ageing : I & A · 2025Review
- The Multifaceted Role of Osteopontin in Modulating the Tumor Microenvironment.Cancer research · 2025Review
- Lifelong restriction of dietary valine has sex-specific benefits for health and lifespan in mice.bioRxiv : the preprint server for biology · 2025Article
- MACanalyzeR scRNAseq analysis tool reveals PPARγNature communications · 2025Article
- Adipose progenitor cell-derived extracellular vesicles suppress macrophage M1 program to alleviate midlife obesity.Nature communications · 2025Article
- The immune duality of osteopontin and its therapeutic implications for kidney transplantation.Frontiers in immunology · 2025Review
- Inflammatory biomarkers as cost-effective predictive tools in metabolic dysfunction-associated fatty liver disease.World journal of gastroenterology · 2024Review
- Osteopontin and Clinical Outcomes in Hemodialysis Patients.Biomedicines · 2024Article
- Air Pollution Drives Macrophage Senescence through a Phagolysosome-15-Lipoxygenase Pathway.ImmunoHorizons · 2024Article
- Senescent skeletal muscle fibroadipogenic progenitors recruit and promote M2 polarization of macrophages.Aging cell · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ATM senescence and its role are unclear in age-related AT dysfunction. Here, we show that ATMs (a) acquire a senescence-like phenotype during chronological aging; (b) display a global decline of basic macrophage functions such as efferocytosis, an essential process to preserve AT homeostasis by clearing dysfunctional or apoptotic cells; and (c) promote AT remodeling and dysfunction. Importantly, we uncover a major role for the age-associated accumulation of osteopontin (OPN) in these processes in visceral AT. Consistently, loss or pharmacologic inhibition of OPN and bone marrow transplantation of OPN-/- mice attenuate the ATM senescence-like phenotype, preserve efferocytosis, and finally restore healthy AT homeostasis in the context of aging. Collectively, our findings implicate pharmacologic OPN inhibition as a viable treatment modality to counter ATM senescence-mediated AT remodeling and dysfunction during aging.
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.