Literature DB >> 30108339

Organ memory: a key principle for understanding the pathophysiology of hypertension and other non-communicable diseases.

Hiroshi Itoh1, Isao Kurihara2, Kazutoshi Miyashita2.   

Abstract

In recent years, several post-interventional analyses of large-scale randomized controlled clinical trials have given us a new concept regarding the risk management of hypertension and cardiovascular diseases. The beneficial effects of intensive treatments were extended even after the interventions ended. This phenomenon is known as "metabolic memory" or "legacy effect", and we recognized its clinical significance. A certain level of evidence in human and animal studies employing organ transplantation techniques has indicated that this type of "memory" resides in each organ and could be transferrable, erasable, and rewritable, which is similar to neuronal and immune "memory". In this review, we define this memory as "organ memory" and summarize the current picture and future direction of this concept. "Organ memory" can be observed in many clinical settings, including in the control of hypertension, diabetes mellitus, and dyslipidemia. Several intensive treatments were demonstrated to have the potential to rewrite "organ memory", leading to the curability of targeted diseases. "Organ memory" is the engraved phenotype of altered organ responsiveness acquired by a time-dependent accumulation of organ stress responses. Not only is the epigenetic change of key genes involved in the formation of "organ memory" but the alteration of multiple factors, including low molecular weight energy metabolites, immune mediators, and tissue structures, is involved as well. These factors intercommunicate during every stress response and carry out incessant remodeling in a certain direction in a spiral fashion through positive feedback mechanisms. Future studies should be directed toward the identification of the core unit of "organ memory" and its manipulation.

Entities:  

Mesh:

Year:  2018        PMID: 30108339     DOI: 10.1038/s41440-018-0081-x

Source DB:  PubMed          Journal:  Hypertens Res        ISSN: 0916-9636            Impact factor:   3.872


  2 in total

1.  Transient Dexamethasone Loading Induces Prolonged Hyperglycemia in Male Mice With Histone Acetylation in Dpp-4 Promoter.

Authors:  Asuka Uto; Kazutoshi Miyashita; Sho Endo; Masaaki Sato; Masaki Ryuzaki; Kenichiro Kinouchi; Masanori Mitsuishi; Shu Meguro; Hiroshi Itoh
Journal:  Endocrinology       Date:  2021-12-01       Impact factor: 5.051

2.  Activation of the intestinal tissue renin-angiotensin system by transient sodium loading in salt-sensitive rats.

Authors:  Masaki Ryuzaki; Kazutoshi Miyashita; Masaaki Sato; Hiroyuki Inoue; Kentaro Fujii; Aika Hagiwara; Asuka Uto; Sho Endo; Takuma Oshida; Kenichiro Kinouchi; Hiroshi Itoh
Journal:  J Hypertens       Date:  2022-01-01       Impact factor: 4.844

  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.