Calvin Yeang

University of California, San Diego

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Sotirios Tsimikas

University of California, San Diego

Joseph L. Witztum

University of California, San Diego

Xiaohong Yang

University of California, San Diego

Christopher K. Glass

University of California, San Diego

Bruno Cotter

UC San Diego Health System

Harpreet S. Bhatia

University of California, San Diego

Ming‐Yow Hung

Taipei Medical University

Michael J. Wilkinson

University of California, San Diego

Jeffrey Kroon

Amsterdam University Medical Centers

Xuchu Que

University of California, San Diego

Cooperative Institutions

University of California, San Diego

Amsterdam University Medical Centers

University of Amsterdam

Academic Medical Center

Brigham and Women's Hospital

Harvard University

UC San Diego Health System

Radboud University Nijmegen

Radboud University Medical Center

SUNY Downstate Health Sciences University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Generation and characterization of LPA-KIV9, a murine monoclonal antibody binding a single site on apolipoprotein (a)

Journal of Lipid Research (2020)

Ayelet Gonen Xiaohong Yang Calvin Yeang Е. А. Алексеева Marlys L. Koschinsky

Lipoprotein (a) [Lp(a)] is a risk factor for CVD and a target of therapy, but Lp(a) measurements are not globally standardized. Commercially available assays generally use polyclonal antibodies that detect multiple sites within the kringle (K)IV

Polyclonal antibodies

Lipoprotein(a)

10.1194/jlr.ra120000830

Cite

Citations (9)

Expression of E06, a natural monoclonal antibody targeted to oxidized phospholipids (OXPL), attenuates the progression of aortic sclerosis in aged hyperlipidemic mice

Atherosclerosis (2016)

Calvin Yeang Ming‐Yow Hung Jennifer Pattison Karen Bowden Nancy D. Dalton

10.1016/j.atherosclerosis.2016.07.212

Cite

Citations (1)

Lipoprotein(a) and oxidized phospholipids in calcific aortic valve stenosis

Current Opinion in Cardiology (2016)

Calvin Yeang Michael J. Wilkinson Sotirios Tsimikas

Purpose of review As the incidence of calcific aortic valve stenosis increases with the aging of the population, improved understanding and novel therapies to reduce its progression and need for aortic valve replacement are urgently needed. Recent findings Lipoprotein(a) is the only monogenetic risk factor for calcific aortic stenosis. Elevated levels are a strong, causal, independent risk factor, as demonstrated in epidemiological, genome-wide association studies and Mendelian randomization studies. Lipoprotein(a) is the major lipoprotein carrier of oxidized phospholipids, which are proinflammatory and promote calcification of vascular cells, two key pathophysiological drivers of aortic stenosis. Elevated plasma lipoprotein(a) and oxidized phospholipids predict progression of pre-existing aortic stenosis and need for aortic valve replacement. The failure of statin trials in pre-existing aortic stenosis may be partially due to an increase in lipoprotein(a) and oxidized phospholipid levels caused by statins. Antisense oligonucleotides targeted to apo(a) are in Phase 2 clinical development and shown to lower both lipoprotein(a) and oxidized phospholipids. Summary Lipoprotein(a) and oxidized phospholipids are key therapeutic targets in calcific aortic stenosis. Strategies aimed at potent lipoprotein(a) lowering to normalize levels and/or to suppress the proinflammatory effects of oxidized phospholipids may prevent progression of this disease.

Mendelian Randomization

Lipoprotein(a)

Proinflammatory cytokine

10.1097/hco.0000000000000300

Cite

Citations (67)

Sphingomyelin biosynthesis: its impact on lipid metabolism and atherosclerosis

Clinical Lipidology (2009)

Xian‐Cheng Jiang Calvin Yeang Zhiqiang Li Mahua Chakraborty Jing Liu

AbstractAbstractThe ability to regulate sphingomyelin (SM) biosynthesis could become a promising treatment for atherosclerosis. SM is one of the major lipid components in plasma and cell membranes. We have found that plasma SM level is an independent risk factor for coronary artery disease. Thus, SM levels have a clinically important impact on lipoprotein metabolism. We have also found that reduction of plasma and liver SM, with concomitant reduction of atherosclerosis, could be achieved by pharmacological inhibition of serine palmitoyltransferase in a mouse model. Moreover, we also found SM synthase 2, the last enzyme for SM biosynthesis, deficiency in macrophages decreases SM levels on plasma membrane and, thus, decreases atherosclerosis in a mouse model. These observations emphasize the need for a better understanding of SM metabolism. This review mainly focuses on the relationship between SM de novo synthesis, lipid metabolism and atherosclerosis.Keywords: atherosclerosischolesterolinsulin resistancelipoproteinsserine palmitoyltransferasesphingomyelinsphingomyelin synthasesphingomyelinrich microdomains (lipid rafts)

Sphingolipid

10.2217/clp.09.49

Cite

Citations (11)

Subcellular Targeting Domains of Sphingomyelin Synthase 1 and 2

Nutrition & Metabolism (2011)

Calvin Yeang Tingbo Ding William J. Chirico Xian‐Cheng Jiang

Abstract Sphingomyelin synthase (SMS) sits at the crossroads of sphingomyelin (SM), ceramide, diacylglycerol (DAG) metabolism. It utilizes ceramide and phosphatidylcholine as substrates to produce SM and DAG, thereby regulating lipid messengers which play a role in cell survival and apoptosis. Furthermore, its product SM has been implicated in atherogenic processes such as retention of lipoproteins in the blood vessel intima. There are two mammalian sphingomyelin synthases: SMS1 and SMS2. SMS1 is found exclusively in the Golgi at steady state, whereas SMS2 exists in the Golgi and plasma membrane. Conventional motifs responsible for protein targeting to the plasma membrane or Golgi are either not present in, or unique to, SMS1 and SMS2. In this study, we examined how SMS1 and SMS2 achieve their respective subcellular localization patterns. Brefeldin A treatment prevented SMS1 and SMS2 from exiting the ER, demonstrating that they transit through the classical secretory pathway. We created truncations and chimeras of SMS1 and SMS2 to define their targeting signals. We found that SMS1 contains a C-terminal Golgi targeting signal and that SMS2 contains a C-terminal plasma membrane targeting signal.

Lipid raft

10.1186/1743-7075-8-89

Cite

Citations (28)

Clonal hematopoiesis driven by DNMT3A and TET2 mutations

Current Opinion in Hematology (2021)

Isidoro Cobo Tiffany Tanaka Christopher K. Glass Calvin Yeang

Purpose of review Clonal hematopoiesis of indeterminate potential (CHIP), defined by the presence of somatic mutations in hematopoietic cells, is associated with advanced age and increased mortality due to cardiovascular disease. Gene mutations in DNMT3A and TET2 are the most frequently identified variants among patients with CHIP and provide selective advantage that spurs clonal expansion and myeloid skewing. Although DNMT3A and TET2 appear to have opposing enzymatic influence on DNA methylation, mounting data has characterized convergent inflammatory pathways, providing insights to how CHIP may mediate atherosclerotic cardiovascular disease (ASCVD). Recent findings We review a multitude of studies that characterize aberrant inflammatory signaling as result of DNMT3A and TET2 deficiency in monocytes and macrophages, immune cells with prominent roles in atherosclerosis. Although specific DNA methylation signatures associated with these known epigenetic regulators have been identified, many studies have also characterized diverse modulatory functions of DNTM3A and TET2 that urge cell and context-specific experimental studies to further define how DNMT3A and TET2 may nonenzymatically activate inflammatory pathways with clinically meaningful consequences. Summary CHIP, common in elderly individuals, provides an opportunity understand and potentially modify age-related chronic inflammatory ASCVD risk.

Proinflammatory cytokine

Source

Cite

Citations (20)

The Effects of Colchicine on Lipoprotein(a) and Oxidized Phospholipid Associated Cardiovascular Disease Risk

European Journal of Preventive Cardiology (2024)

Niekbachsh Mohammadnia Amber van Broekhoven Willem A. Bax John W. Eikelboom Arend Mosterd

Abstract Aims Inflammatory lipoprotein(a) [Lp(a)] and oxidized phospholipids (OxPLs) on lipoproteins convey residual cardiovascular disease risk. The low-dose colchicine 2 (LoDoCo2) trial showed that colchicine reduced the risk of cardiovascular events occurring on standard therapies in patients with chronic coronary syndrome (CCS). We explored the effects of colchicine on Lp(a)- and oxidized lipoprotein-associated risk in a LoDoCo2 biomarker subpopulation. Methods and results Lipoprotein(a) and OxPLs on apolipoprotein(a) [OxPL-apo(a)] and apolipoprotein B-100 (OxPL-apoB) levels were determined in the biomarker population of the LoDoCo2 trial (n = 1777). The Cox regression analysis was used to compare the risk of the primary endpoint, consisting of myocardial infarction, ischaemic stroke, or ischaemia-driven revascularization by biomarker levels. Interactions between treatment, Lp(a), and OxPL levels were evaluated. Lipoprotein(a), OxPL-apo(a), and OxPL-apoB levels were similar between the colchicine and placebo groups. Consistent risk reduction by colchicine was observed in those with Lp(a) < 125 nmol/L and ≥125 nmol/L and the highest OxPL-apo(a) tertile compared with the lowest (Pinteraction = 0.92 and 0.66). The absolute risk reduction for those with Lp(a) ≥ 125 nmol/L appeared higher compared with those with Lp(a) < 125 nmol/L (4.4% vs. 2.4%). A treatment interaction for colchicine was found in those with the highest OxPL-apoB tertile vs. the lowest (Pinteraction = 0.04). Conclusion In patients with CCS, colchicine reduces cardiovascular disease risk in those with and without elevated Lp(a) but absolute benefits appeared higher in those with Lp(a) ≥ 125 nmol/L. Patients with higher levels of OxPL-apoB experienced greater benefit of colchicine, suggesting that colchicine may be more effective in subjects with heightened oxidation-driven inflammation.

Colchicine

Atherosclerotic cardiovascular disease

Lipoprotein(a)

10.1093/eurjpc/zwae355

Cite

Citations (2)

LDL-C CORRECTED FOR DIRECTLY MEASURED LIPOPROTEIN(A)-CHOLESTEROL IN PATIENTS TREATED WITH LIPOPROTEIN APHERESIS

Journal of the American College of Cardiology (2022)

Calvin Yeang Anne P. Nugent Fei Su Brian Dinh Sotirios Tsimikas

Lipoprotein(a)

LDL apheresis

10.1016/s0735-1097(22)02036-8