New data show that the mINDY gene is involved in blood pressure regulation

Authors from the German Diabetes Research Center (DZD) provided data showing that Indy mammalian long-lived gene (mINDY) is involved in the regulation of blood pressure in the A look at the Journal of Clinical Research (JCI).

It has now been shown to reduce mINDY, which is known to extend life expectancy in lower organisms and to prevent diet-induced obesity, liver fat, and insulin resistance. in mice, lowering blood pressure and heart rate in rodents.

The authors provided mechanical insight into the basic psychology apparatus based on in vivo data in a genetic collision model as well as microarray and in vitro studies.

In addition, the hypothesis is supported by the detection of acute in vitro effects using a small molecular inhibitor of mINDY. The authors conclude that elimination of mIndy replicates beneficial cardiovascular and metabolic responses to caloric restriction, making it an attractive therapeutic target.

Andreas Birkenfeld and colleagues present a comprehensive study showing that mIndy elimination reduces sympathoadrenal support for lower blood pressure and arterial hypertension and heart rate in a neck stroke model. Blood pressure was aggressively assessed using intra-arterial pressure probes over several days.

Urinary analysis for catecholamines and metanephrines as well as noninvasive transcriptional analysis of adrenal glands identified the affected biosynthetic pathways. Indeed, catecholamine biosynthesis was reduced in mINDY-KO adrenals, but plasma steroids and steroid hormone synthesis had no effect.

In vitro studies of adrenal cell line supported this hypothesis. MIndy codes for which is a carboxylic acid transport protein expressed in the plasma membrane. Citrate, the main substrate of the mINDY transporter, increased catecholamine content, while pharmacological inhibition of mINDY by a small molecule inhibitor affected it.

The study provided further insight into the psychological mechanisms of the beneficial effects of reducing mINDY activity known to protect against diet and metabolic diseases caused by getting older with devices that are similar to caloric restriction.

Thus, the modern mechanical data showed an increase in cardiometabolic cross-linking and support for mINDY as a promising target for the full spectrum of metabolic syndrome components, including increased blood pressure.