ArticleCardiovascular research2014
Bone marrow deficiency of TRPC3 channel reduces early lesion burden and necrotic core of advanced plaques in a mouse model of atherosclerosis.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
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- Identification of critical endoplasmic reticulum stress-related genes in advanced atherosclerotic plaque.Scientific reports · 2025Article
- Transient receptor potential channels as key regulators of cell death in atherosclerosis.Frontiers in immunology · 2025Review
- Tension at the gate: sensing mechanical forces at the blood-brain barrier in health and disease.Journal of neuroinflammation · 2024Review
- The Multifaceted Nature of Macrophages in Cardiovascular Disease.Biomedicines · 2024Review
- Role of TRP Channels in Metabolism-Related Diseases.International journal of molecular sciences · 2024Review
- Mechanosensing and Mechanosignal Transduction in Atherosclerosis.Current atherosclerosis reports · 2023Review
- TRP (transient receptor potential) ion channel family: structures, biological functions and therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- Function of TRP channels in monocytes/macrophages.Frontiers in immunology · 2023Review
- The role of macrophage ion channels in the progression of atherosclerosis.Frontiers in immunology · 2023Review
- Six Decades of History of Hypertension Research at the University of Toledo: Highlighting Pioneering Contributions in Biochemistry, Genetics, and Host-Microbiota Interactions.Current hypertension reports · 2022Review
- Role of mechanosensitive channels/receptors in atherosclerosis.American journal of physiology. Cell physiology · 2022Review
- The contribution of ion channels to shaping macrophage behaviour.Frontiers in pharmacology · 2022Review
- miR-454-3p prevents ox-LDL-induced apoptosis in HAECs by targeting TRPC3.Experimental and therapeutic medicine · 2021Article
- Review
- TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020Review
- Macrophage autophagy regulates mitochondria-mediated apoptosis and inhibits necrotic core formation in vulnerable plaques.Journal of cellular and molecular medicine · 2020Article
- Ibudilast attenuates doxorubicin-induced cytotoxicity by suppressing formation of TRPC3 channel and NADPH oxidase 2 protein complexes.British journal of pharmacology · 2019Article
- Ablating astrocyte insulin receptors leads to delayed puberty and hypogonadism in mice.PLoS biology · 2019Article
- Reduced calcification and osteogenic features in advanced atherosclerotic plaques of mice with macrophage-specific loss of TRPC3.Atherosclerosis · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
aimsMacrophage apoptosis plays a determinant role in progression of atherosclerotic lesions. An important goal in atherosclerosis research is to identify new components of macrophage apoptosis that can eventually be exploited as molecular targets in strategies aimed at manipulating macrophage function in the lesion. In the previous work from our laboratory, we have shown that transient receptor potential canonical 3 (TRPC3) channel is an obligatory component of survival mechanisms in human and murine macrophages and that TRPC3-deficient non-polarized bone marrow-derived macrophages exhibit increased apoptosis, suggesting that in vivo TRPC3 might influence lesion development. In the present work, we used a bone marrow transplantation strategy as a first approach to examine the impact of macrophage deficiency of TRPC3 on early and advanced atherosclerotic lesions of Apoe(-/-) mice. METHODS AND
resultsAfter 3 weeks of high-fat diet, lesions in mice transplanted with bone marrow from Trpc3(-/-) donors were smaller and with reduced cellularity than controls. Advanced lesions from these mice exhibited reduced necrotic core, less apoptotic macrophages, and increased collagen content and cap thickness. In vitro, TRPC3-deficient macrophages polarized to the M1 phenotype showed reduced apoptosis, whereas both M1 and M2 macrophages had increased efferocytic capacity.
conclusionsBone marrow deficiency of TRPC3 has a dual beneficial effect on lesion progression by reducing cellularity at early stages and necrosis in the advanced plaques. Our findings represent the first evidence for a role of a member of the TRPC family of cation channels in mechanisms associated with atherosclerosis.
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Registered trials
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