ArticleThe Journal of clinical investigation2017
CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 107 citations in OpenAlex.
- Antibody-lectin chimeras for glyco-immune checkpoint blockade.Nature biotechnology · 2026Article
- Myeloid Cell-Specific Deletion of LGR4 Suppresses Atherosclerotic Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Gut Microbiota and Atherosclerotic Plaque Instability: Cellular and Molecular Mechanisms.International journal of molecular sciences · 2026Review
- A Road Map to Understanding Cardiovascular Disease in Diabetes: From the AHA Strategically Focused Research Network in Cardiometabolic Health and Type 2 Diabetes.Circulation research · 2026Review
- How Advanced is Nanomedicine to Treat Atherosclerosis? A Comprehensive Review of the Literature.International journal of nanomedicine · 2026Review
- LncRNA SCARNA8 promotes atherosclerotic plaque instability by inhibiting macrophage efferocytosis.Epigenetics · 2025Article
- Efferocytosis: the art of cellular clearance and novel perspectives in disease therapy.Molecular cancer · 2025Review
- Activated protein C ameliorates diabetes-induced atherosclerosis by sustaining macrophage efferocytosis.Cardiovascular diabetology · 2025Article
- Nanoparticle Drug Delivery Systems for Atherosclerosis: Precision Targeting, Inflammatory Modulation, and Plaque Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- A New Approach to the Diagnosis and Treatment of Cardiovascular Diseases.Pharmaceutics · 2025Review
- Impaired CAMK4 Activity Limits Atherosclerosis and Reprograms Myelopoiesis.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Electroacupuncture improves cardiac function in hyperlipidemic rats by enhancing efferocytosis in myocardial macrophages via the PPARγ-LXRα-MerTK pathway.Journal of traditional and complementary medicine · 2025Article
- Clearing the Path: Exploring Apoptotic Cell Clearance in Inflammatory and Autoimmune Disorders for Therapeutic Advancements.Molecular biotechnology · 2025Review
- Exploring the Roles of Liver X Receptors in Lipid Metabolism and Immunity in Atherosclerosis.Biomolecules · 2025Review
- Anti-Inflammatory Lipid Mediators from Polyunsaturated Fatty Acids: Insights into their Role in Atherosclerosis Microenvironments.Current atherosclerosis reports · 2025Review
- The Atherosclerotic Plaque Microenvironment as a Therapeutic Target.Current atherosclerosis reports · 2025Review
- The Role of Macrophages in Atherosclerosis: Participants and Therapists.Cardiovascular drugs and therapy · 2025Review
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- Emerging Gene Therapy Based on Nanocarriers: A Promising Therapeutic Alternative for Cardiovascular Diseases and a Novel Strategy in Valvular Heart Disease.International journal of molecular sciences · 2025Review
- Efferocytosis: The Janus-Faced Gatekeeper of Aging and Tumor Fate.Aging cell · 2025Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase γ (CaMKIIγ) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. Western diet-fed LDL receptor-deficient (Ldlr-/-) mice with myeloid-specific deletion of CaMKII had smaller necrotic cores with concomitantly thicker collagen caps. These lesions demonstrated evidence of enhanced efferocytosis, which was associated with increased expression of the macrophage efferocytosis receptor MerTK. Mechanistic studies revealed that CaMKIIγ-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIγ had increased expression of the transcription factor ATF6. We determined that ATF6 induces liver X receptor-α (LXRα), an Mertk-inducing transcription factor, and that increased MerTK expression and efferocytosis in CaMKIIγ-deficient macrophages is dependent on LXRα. These findings identify a macrophage CaMKIIγ/ATF6/LXRα/MerTK pathway as a key factor in the development of necrotic atherosclerotic plaques.
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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.