Evidence map›Paper›PMID 22227126›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2012

The renin-angiotensin system: a target of and contributor to dyslipidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome.

Kelly Putnam, Robin Shoemaker, Frederique Yiannikouris, Lisa A Cassis

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
16.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.

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  10. Epigenetic Modulation of the ACE System Underlies the Slow Aerobic Muscle Phenotype and Metabolic Exercise Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Kelly PutnamGraduate Center for Nutritional Sciences, University of Kentucky, Lexington, 40536-0200, USA.
Robin Shoemaker
Frederique Yiannikouris
Lisa A Cassis
University of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
THROMBOSPONDIN1 MEDIATES MACROPHAGE INFILTRATION INTO ADIPOSE TISSUE AND PROMOTEP20RR021954 · NCRR · UNIVERSITY OF KENTUCKY · PI ECKHARDT, ERIK · 2008 to 2011
$8.3M
Angiotensin: A Link Between Obesity and HypertensionR01HL073085 · NHLBI · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2003 to 2017
$5.0M
NCRR NIH HHS P20 RR021954NCRR NIH HHS P20-RR-021954NHLBI NIH HHS HL-073085NHLBI NIH HHS R01 HL073085NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) is an important therapeutic target in the treatment of hypertension. Obesity has emerged as a primary contributor to essential hypertension in the United States and clusters with other metabolic disorders (hyperglycemia, hypertension, high triglycerides, low HDL cholesterol) defined within the metabolic syndrome. In addition to hypertension, RAS blockade may also serve as an effective treatment strategy to control impaired glucose and insulin tolerance and dyslipidemias in patients with the metabolic syndrome. Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. An activated local RAS in these cell types may contribute to dysregulated function by promoting oxidative stress, apoptosis, and inflammation. This review will discuss data demonstrating the regulation of components of the RAS by cholesterol and its metabolites, glucose, and/or insulin in cell types implicated in disorders of the metabolic syndrome. In addition, we discuss data supporting a role for an activated local RAS in dyslipidemias and glucose intolerance/insulin resistance and the development of hypertension in the metabolic syndrome. Identification of an activated RAS as a common thread contributing to several disorders of the metabolic syndrome makes the use of angiotensin receptor blockers and ACE inhibitors an intriguing and novel option for multisymptom treatment.

Indexed as

Renin-Angiotensin SystemAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersAnimalsBlood GlucoseBlood PressureDyslipidemiasGlucose Metabolism DisordersHomeostasisHumansHypertensionInsulin ResistanceLipid MetabolismMetabolic SyndromeAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersBlood Glucose

Identifiers

PMID22227126
PMCPMC3311482
OpenAlexW2137543153

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.