Ang II induces DNA methylation and p53 activation to regulate miR-150-5p in hypertension progression

Bian, Qian; Ding, Zhiwen; Xu, Ran; Zhao, Jing; Zou, Yunzeng

doi:10.1016/j.yjmcc.2019.11.106

Cited by 1 publication

(1 citation statement)

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“…Also, some of the epigenetic modifications associated with diabetic nephropathy in type 2 diabetic db/db mice were reversed by losartan treatment, pointing to the involvement of AT1R in the induction of chromatin changes that affect the expression of harmful genes (Reddy et al., 2014 ). In addition, in cultured AC16 cardiomyocytes, Ang II prompted DNA methylation of the MIR150HG gene, thereby reducing the expression of miR‐150‐5p microRNA which enhanced AT1R expression (Qian et al., 2019 ). Moreover, in cultured atrial cardiomyocytes, Ang II stimulated nuclear export of histone deacetylase 4 and 5 (HDAC4 and HDAC5) into the cytoplasm—which inhibits chromatin condensation—and allowed the epigenetic transcription of hypertrophy‐related genes.…”

Section: Epigenetics and Agingmentioning

confidence: 99%

Renin–angiotensin system inhibitors positively impact on multiple aging regulatory pathways: Could they be used to protect against human aging?

de Cavanagh,

Inserra,

Ferder

2024

Physiological Reports

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The renin–angiotensin system (RAS)—a classical blood pressure regulator—largely contributes to healthy organ development and function. Besides, RAS activation promotes age‐related changes and age‐associated diseases, which are attenuated/abolished by RAS‐blockade in several mammalian species. RAS‐blockers also increase rodent lifespan. In previous work, we discussed how RAS‐blockade downregulates mTOR and growth hormone/IGF‐1 signaling, and stimulates AMPK activity (together with klotho, sirtuin, and vitamin D‐receptor upregulation), and proposed that at least some of RAS‐blockade's aging benefits are mediated through regulation of these intermediaries and their signaling to mitochondria. Here, we included RAS‐blockade's impact on other aging regulatory pathways, that is, TGF‐ß, NF‐kB, PI3K, MAPK, PKC, Notch, and Wnt, all of which affect mitochondria. No direct evidence is available on RAS/RAS‐blockade‐aging regulatory pathway–mitochondria interactions. However, existing results allow to conjecture that RAS‐blockers neutralize mitochondrial dysfunction by acting on the discussed pathways. The reviewed evidence led us to propose that the foundation is laid for conducting clinical trials aimed at testing whether angiotensin‐converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB)—even at subclinical doses—offer the possibility to live longer and in better health. As ACEi and ARB are low cost and well‐tolerated anti‐hypertension therapies in use for over 35 years, investigating their administration to attenuate/prevent aging effects seems simple to implement.

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Section: Epigenetics and Agingmentioning

confidence: 99%