ReviewInternational journal of biological sciences2025
The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.
Review in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed.
- Dual-targeted engineered mesenchymal stem cell-derived extracellular vesicles delivering Nedd4 attenuate renal fibrosis in diabetic kidney disease.Materials today. Bio · 2026Article
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- Article
- Gut microbial-derived metabolites: key players in kidney disease and renal fibrosis.International journal of biological sciences · 2026Review
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- Metformin Mitigates Diabetes-Driven Renal Senescence via Immunomodulation and the FABP4/FOXO1 Axis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Immune-mediated interactions between sarcopenia and atherosclerosis in aging.Immunity & ageing : I & A · 2025Review
- Macrophage derived VEGF regulates macrophage senescence to inhibit radiation-induced dermatitis.Journal of translational medicine · 2025Article
- Influence of a Zombie-like State of the Liver on Drugs and Its Medico-Legal Implications: A Scoping Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Macrophage Depletion Alleviates Immunosenescence in Diabetic Kidney by Modulating GDF-15 and Klotho.International journal of molecular sciences · 2025Article
- The anti-aging potential of antihypertensive peptides ofFrontiers in aging · 2025Article
- Astragaloside IV Improves Diabetic Kidney Disease by Regulating NLRP3 Inflammasome.Journal of diabetes research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a complex biological process that involves the gradual decline of cellular, tissue, and organ functions. In kidney, aging manifests as tubular atrophy, glomerulosclerosis, and progressive renal function decline. The critical role of senescence-associated macrophage in diseases, particularly kidney diseases, is increasingly recognized. During this process, macrophages exhibit a range of pro-damage response to senescent tissues and cells, while the aging of macrophages themselves also significantly influences disease progression, creating a bidirectional regulatory role between aging and macrophages. To explore this bidirectional mechanism, this review will elucidate the origin, characteristic, phenotype, and function of macrophages in response to the senescence-associated secretory phenotype (SASP), extracellular vesicles from senescent cells, and the senescence cell-engulfment suppression (SCES), particularly in the context of kidney disease. Additionally, it will discuss the characteristics of senescent macrophage, such as common markers, and changes in autophagy, metabolism, gene regulation, phagocytosis, antigen presentation, and exosome secretion, along with their physiological and pathological impacts on renal tissue cells. Furthermore, exploring therapies and drugs that modulate the function of senescent macrophages or eliminate senescent cells may help slow the progression of kidney aging and damage.
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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.