ArticleAmerican journal of physiology. Cell physiology2015
Secreted protein acidic and rich in cysteine facilitates age-related cardiac inflammation and macrophage M1 polarization.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Guidelines for authors and reviewers on antibody use in physiology studies.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Identifying Potential Candidate Hub Genes and Functionally Enriched Pathways in the Immune Responses to Quadrivalent Inactivated Influenza Vaccines in the Elderly Through Co-Expression Network Analysis.Frontiers in immunology · 2020Trial
- Endothelial cell-microglia crosstalk mediates heart failure-associated synaptic loss and cognitive impairment in male mice.Nature communications · 2026Article
- Predictive value of 1-hour postprandial SPARC levels on metabolic outcomes from Mediterranean diet adherence: results from a randomized controlled feeding study.Life metabolism · 2026Article
- Inflammaging and Cardiovascular Risk in Old Women.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- The role of glucose metabolic reprogramming in myocarditis and advances in therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Exploring the Role of SPARC in Atherosclerosis: Mechanisms and Potential Implications.Current atherosclerosis reports · 2025Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Potential of biomarkers of ageing in predicting severity of influenza virus infection and vaccination efficacy.npj aging · 2025Review
- Secreted Protein Acidic and Rich in Cysteine (SPARC) Induced by the Renin-Angiotensin System Causes Endothelial Inflammation in the Early Stages of Hypertensive Vascular Injury.International journal of molecular sciences · 2025Article
- SPARC: a key mediator of apoptosis in human umbilical vein endothelial cells and its role in hypertension mechanism.In vitro cellular & developmental biology. Animal · 2025Article
- Systematic Mendelian Randomization Exploring Druggable Genes for Hemorrhagic Strokes.Molecular neurobiology · 2025Article
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- Matricellular proteins in immunometabolism and tissue homeostasis.BMB reports · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Suppression of SPARC Ameliorates Ovalbumin-induced Airway Remodeling via TGFβ1/Smad2 in Chronic Asthma.Allergy, asthma & immunology research · 2024Article
- Reduction of SPARC protects mice against NLRP3 inflammasome activation and obesity.The Journal of clinical investigation · 2023Article
- Review
- Plasma SPARC Elevation in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
To investigate the role of secreted protein acidic and rich in cysteine (SPARC) in age-related cardiac inflammation, we studied six groups of mice: young (3-5 mo old), middle-aged (10-12 mo old), and old (18-29 mo old) C57BL/6 wild-type (WT) and SPARC-null (Null) mice (n = 7-10/group). Cardiac function and structure were determined by echocardiography. The left ventricle was used for cytokine gene array and macrophage quantification by immunohistochemistry. Macrophage infiltration increased with age in WT (n = 5-6/group, P < 0.05 for young vs. old), but not in Null. Proinflammatory markers (Ccl5, Cx3cl1, Ccr2, and Cxcr3) increased in middle-aged and old WT, whereas they were increased only in old Null compared with respective young (n = 5-6/group, P < 0.05 for all). These results suggest that SPARC deletion delayed age-related cardiac inflammation. To further assess how SPARC affects inflammation, we stimulated peritoneal macrophages with SPARC (n = 4). SPARC treatment increased expression of proinflammatory macrophage M1 markers and decreased anti-inflammatory M2 markers. Echocardiography (n = 7-10/group) revealed an age-related increase in wall thickness of the left ventricle in WT (0.76 ± 0.02 mm in young vs. 0.91 ± 0.03 mm in old; P < 0.05) but not in Null (0.78 ± 0.01 mm in young vs. 0.84 ± 0.02 mm in old). In conclusion, SPARC deletion delayed age-related increases in macrophage infiltration and proinflammatory cytokine expression in vivo and in vitro. SPARC acts as an important mediator of age-related cardiac inflammation by increasing the expression of macrophage M1 markers and decreasing M2 markers.
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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 OpenQuestion graph.