Research summary
Lipoprotein metabolism, cardiovascular risk, and genetic predisposition to atherosclerotic disease organise this corpus. The 2004 NEJM PROVE-IT-style intensive vs moderate statin paper enrolled 4,162 patients hospitalised for acute coronary syndromes within the preceding 10 days and compared 40 mg pravastatin daily (standard) with 80 mg atorvastatin daily (intensive), with a composite primary endpoint of death, MI, documented unstable angina requiring rehospitalisation, late revascularisation, and stroke [1]. The 2011 NEJM cholesterol-efflux paper measured cholesterol efflux capacity in 203 healthy volunteers (with carotid IMT assessment), 442 patients with angiographically confirmed CAD, and 351 without confirmed CAD using a validated ex-vivo macrophage system with apolipoprotein-B-depleted serum, framing efflux capacity as a marker of HDL function and atherosclerotic burden independent of HDL-C concentration [2]. The 2005 Circulation Research review consolidates regulation of HDL metabolism and reverse cholesterol transport (RCT), covering HDL synthesis, intravascular remodelling, catabolism, and the role of HDL in promoting cholesterol efflux from peripheral tissues and transport to the liver [6]. The 2003 NEJM low-carbohydrate-diet trial randomised 63 obese men and women to a low-carbohydrate, high-protein, high-fat (Atkins) diet versus a conventional low-calorie, high-carbohydrate, low-fat diet with one-year follow-up, reporting larger weight loss at 3 and 6 months on the low-carbohydrate arm [3]. The 2007 Science paper on chromosome 9p21 reports an association between a common sequence variant adjacent to CDKN2A and CDKN2B and myocardial infarction in 4,587 cases and 12,767 controls, with homozygotes (~21% of the population) at 1.64× the noncarrier risk and 2.02× for early-onset cases [4]. The 2016 NEJM paper quantified polygenic CAD risk in 7,814 ARIC, 21,222 WGHS, 22,389 MDCS, and 4,260 BioImage participants, and assessed how adherence to a healthy lifestyle attenuates that genetic risk [5]. Across the six works the through-line is the integration of lipid-lowering pharmacology [1], HDL biology [2,6], dietary intervention [3], common-variant genetic risk [4], and polygenic risk-stratification [5] within a single cardiovascular-disease research programme.
Recent publications
- Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary SyndromesDOI
- Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetesDOI
- Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and AtherosclerosisDOI
- A Randomized Trial of a Low-Carbohydrate Diet for ObesityDOI
- A Common Variant on Chromosome 9p21 Affects the Risk of Myocardial InfarctionDOI
- Genetic Risk, Adherence to a Healthy Lifestyle, and Coronary DiseaseDOI
- Assessment of Coronary Artery Disease by Cardiac Computed TomographyDOI
- From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locusDOI
- A variant in CDKAL1 influences insulin response and risk of type 2 diabetesDOI
- New Insights Into the Regulation of HDL Metabolism and Reverse Cholesterol TransportDOI
The lab page does not clearly state student acceptance status. Email the professor directly to confirm.
How to apply
Email Daniel J. Rader 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
For applications via MEXT scholarship: see our MEXT 2027 complete guide and university-specific University Recommendation track.
External profiles
- ORCID: https://orcid.org/0000-0002-9245-9876
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, The University of Tokyo faculty directory). Last refreshed 2026-05. Report incorrect information.