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Angiotensin type 1 receptor modulates macrophage polarization and renal injury in obesity

Li-Jun Ma1, Bridgette A Corsa, Jun Zhou

  • 1Department of Pathology, Vanderbilt Univ. Medical Center, Nashville, TN 37232-2561, USA. Lijun.ma@vanderbilt.edu

American Journal of Physiology. Renal Physiology
|March 4, 2011
PubMed

Insights

Obesity accelerates kidney injury by increasing inflammation and shifting macrophage balance towards a proinflammatory state. Blocking the angiotensin type 1 receptor reduces these harmful effects in obese mice.

Area of Science:

  • Nephrology
  • Metabolic Diseases
  • Immunology

Background:

  • Obesity is a risk factor for chronic kidney disease (CKD), but mechanisms are unclear.
  • The renin-angiotensin system plays a role in both obesity and CKD.
  • Angiotensin type 1 (AT(1)) receptor subtypes (AT(1a) and AT(1b)) are key components.

Purpose of the Study:

  • Investigate the role of the AT(1a) receptor in high-fat diet (HFD)-induced obesity and kidney injury.
  • Determine the impact of AT(1) receptor blockade on obesity-related renal inflammation and macrophage polarization.

Main Methods:

  • Used wild-type (WT) and AT(1a) knockout (AT1aKO) mice fed a HFD for 24 weeks.
  • Assessed metabolic parameters, body composition, and kidney histology.
  • Analyzed kidney and adipose tissue macrophage infiltration and M1/M2 polarization markers.
  • Administered an AT(1) receptor blocker to obese WT mice.

Main Results:

  • HFD induced obesity, insulin resistance, and kidney injury (mesangial expansion, tubular vacuolization) in WT mice.
  • AT1aKO mice had altered body fat and cholesterol but similar weight gain and kidney injury compared to obese WT mice.
  • Both obese groups showed increased kidney macrophage infiltration and M1 markers; AT1aKO mice had heightened abnormalities and increased AT(1b) expression.
  • AT(1) receptor blockade reduced renal macrophage infiltration, M1 markers, and promoted M2 markers in obese WT mice.

Conclusions:

  • Obesity exacerbates kidney injury through increased inflammation in adipose and kidney tissues.
  • A proinflammatory shift in macrophage M1/M2 balance contributes to obesity-related kidney damage.
  • Targeting the AT(1) receptor may mitigate obesity-induced kidney injury by modulating inflammation.

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