by Denise Karounos

With Valentine’s Day observed this Friday in some countries, the theme of this PepTalk is close to the heart.   A new publication takes a look at antimicrobial peptides and cardiac hypertrophy. Cardiac hypertrophy is the enlargement of the heart and can be caused by several factors, including hypertension, congenital heart disease, exercise, pregnancy, injury, or stress.  In itself, it is not always a bad thing, but when brought on by disease, it can further evolve into heart failure and mortality.  In a new publication in Cell Death & Disease, a team, led by Xiaofang Wang of Zhengzhou University, investigated the effects of the cathelicidin-related antimicrobial peptides and cardiac hypertrophy induced by pressure overload. As a part of the innate defense system of organisms, host defense peptides provide a variety of protections, including antibacterial activity, cell signaling, promoting wound healing, and other immunomodulatory actions.  Among these peptides are the cathelicidins, a family of antimicrobial peptides including LL-37 in humans, cathelicidin-related antimicrobial peptide (CRAMP) in mice, and pig myeloid antibacterial peptide 36 (PMAP-36), and CATH-2 in chickens.  Wang and team found that in mice, CRAMP levels increased in the early stages of cardiac hypertrophy and decreased as heart failure progressed. When they suppressed its expression, the severity of the enlargement increased.   They also noticed that CRAMP was anti-oxidative stress and anti-inflammation.1 Read more about their intriguing work here.  

Reference:

  1. X. Wang et al., Cell Death & Disease, 11(96), 1 (2020).

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Tagged antimicrobial peptides cardiac hypertrophy heart disease host defense peptides hypertension Vivitide