ArticleAmerican journal of physiology. Heart and circulatory physiology2021
SPARC production by bone marrow-derived cells contributes to myocardial fibrosis in pressure overload.
Article in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Mechanical stretch reduces fibroblast activation in heart failure with reduced ejection fraction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF.Experimental & molecular medicine · 2026Article
- Natural language processing of biomedical text to map and prioritize protein-disease associations in HFpEF.Computers in biology and medicine · 2026Article
- Connective tissue disorders and cardiac arrhythmias: genetic pathways, mechanistic bridges, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- 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
- Persistent Fibrosis in Heart Failure With a Reduced Ejection Fraction Linked to Phenotypic Differences in Human Cardiac Fibroblast Populations.Journal of the American Heart Association · 2025Article
- Macrophages in the infarcted heart acquire a fibrogenic phenotype, expressing matricellular proteins, but do not undergo fibroblast conversion.Journal of molecular and cellular cardiology · 2024Article
- The Extracellular Matrix and Cardiac Pressure Overload: Focus on Novel Treatment Targets.Cells · 2024Review
- Role of macrophages in regression of myocardial fibrosis following alleviation of left ventricular pressure overload.American journal of physiology. Heart and circulatory physiology · 2024Article
- Gingival proteomics reveals the role of TGF beta and YAP/TAZ signaling in Raine syndrome fibrosis.Scientific reports · 2024Article
- Suppression of SPARC Ameliorates Ovalbumin-induced Airway Remodeling via TGFβ1/Smad2 in Chronic Asthma.Allergy, asthma & immunology research · 2024Article
- Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction.Journal of cardiovascular development and disease · 2023Article
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- Article
- Secreted Protein Acidic and Rich in Cysteine Mediates the Development and Progression of Diabetic Retinopathy.Frontiers in endocrinology · 2022Article
- From Systemic Inflammation to Myocardial Fibrosis: The Heart Failure With Preserved Ejection Fraction Paradigm Revisited.Circulation research · 2021Review
- Secreted Protein Acidic and Rich in Cysteine as A Regeneration Factor: Beyond the Tissue Repair.Life (Basel, Switzerland) · 2021Article
- Titanium Nanoparticles Enhance Production and Suppress Stabilin-1-Mediated Clearance of GDF-15 in Human Primary Macrophages.Frontiers in immunology · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
In human heart failure and in murine hearts with left-ventricular pressure overload (LVPO), increases in fibrosis are associated with increases in myocardial stiffness. Secreted protein acidic and rich in cysteine (SPARC) is shown to be necessary for both cardiac fibrosis and increases in myocardial stiffness in response to LVPO; however, cellular sources of cardiac SPARC are incompletely defined. Irradiation and bone marrow transfer were undertaken to test the hypothesis that SPARC expression by bone marrow-derived cells is an important mediator of fibrosis in LVPO. In recipient SPARC-null mice transplanted with donor wild-type (WT) bone marrow and subjected to LVPO, levels of fibrosis similar to that of WT mice were found despite the lack of SPARC expression by resident cells. In recipient WT mice with donor SPARC-null bone marrow, significantly less fibrosis versus that of WT mice was found despite the expression of SPARC by resident cells. Increases in myocardial stiffness followed a similar pattern to that of collagen deposition. Myocardial macrophages were significantly reduced in SPARC-null mice with LVPO versus that of WT mice. Recipient SPARC-null mice transplanted with donor WT bone marrow exhibited an increase in cardiac macrophages versus that of SPARC-null LVPO and donor WT mice with recipient SPARC-null bone marrow. Expression of vascular cellular adhesion molecule (VCAM), a previously identified binding partner of SPARC, was assessed in all groups and with the exception of WT mice, increases in VCAM immunoreactivity with LVPO were observed. However, no differences in VCAM expression between bone marrow transplant groups were noted. In conclusion, SPARC expression by bone marrow-derived cells was critical for fibrotic deposition of collagen and influenced the expansion of myocardial macrophages in response to LVPO.
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