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The Transcription Factor c-Myb Worsens Atherosclerosis


A recent study has outlined the relationship between B cells, atherosclerosis, and the transcription factor c-Myb. While this factor is necessary for hematopoiesis, the formation of new blood cells, it has been shown to affect B cells, a type of lymphocyte, in a way that makes atherosclerosis more severe.

A new look at inflammaging

Inflammation can have beneficial effects in the short term, but chronic, long-term inflammation is known to exacerbate serious diseases. With age, the immune system falters and constantly reacts to things that it sees as threats, thus leading to the rise in chronic inflammation known as inflammaging. In the case of atherosclerosis, the relationship between cholesterol and immune cells plays a major role in making things worse [1].

In this study, researchers have shown that the transcription factor c-Myb contributes to this problem. c-Myb is necessary for the production of red blood cells, and mice without this factor die before they are born. However, as this study shows, atherosclerosis-prone mice that only produce half as much c-Myb as normal have a less aggressive B cell response, reducing their susceptibility to this dangerous disease.

The researchers also note that reducing c-Myb increases the number of IgM antibodies against oxidized low-density lipoprotein, one of the direct causes of atherosclerosis; this is additional evidence that modulating this factor may be beneficial.


Mechanisms that govern transcriptional regulation of inflammation in atherosclerosis remain largely unknown. Here, we identify the nuclear transcription factor c-Myb as an important mediator of atherosclerotic disease in mice. Atherosclerosis-prone animals fed a diet high in cholesterol exhibit increased levels of c-Myb in the bone marrow. Use of mice that either harbor a c-Myb hypomorphic allele or where c-Myb has been preferentially deleted in B cell lineages revealed that c-Myb potentiates atherosclerosis directly through its effects on B lymphocytes. Reduced c-Myb activity prevents the expansion of atherogenic B2 cells yet associates with increased numbers of IgM-producing antibody-secreting cells (IgM-ASCs) and elevated levels of atheroprotective oxidized low-density lipoprotein (OxLDL)-specific IgM antibodies. Transcriptional profiling revealed that c-Myb has a limited effect on B cell function but is integral in maintaining B cell progenitor populations in the bone marrow. Thus, targeted disruption of c-Myb beneficially modulates the complex biology of B cells in cardiovascular disease.


Our immune systems are governed by an intricately complicated set of chemical signals. Things that are beneficial in some cases, such as inflammation, are decisively detrimental in others. It is possible that if we can modulate the immune system’s ongoing, counterproductive response to long-term problems, such as by reducing c-Myb, we may potentially be able to reduce the prevalence and severity of age-related diseases while we work towards a future in which these diseases are completely curable.

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[1] Tall, A. R., & Yvan-Charvet, L. (2015). Cholesterol, inflammation and innate immunity. Nature Reviews Immunology, 15(2), 104.

About the author
Josh Conway

Josh Conway

Josh is a professional editor and is responsible for editing our articles before they become available to the public as well as moderating our Discord server. He is also a programmer, long-time supporter of anti-aging medicine, and avid player of the strange game called “real life.” Living in the center of the northern prairie, Josh enjoys long bike rides before the blizzards hit.
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