Live longer sans the AT1A receptor.
Excessive activation of the AT(1A) receptor (AT(1A)R) by angiotensin II (Ang II) is implicated in the age-related development of hypertension, diabetes, and kidney disease. AT(1A)R-deficient mice live longer and have lower levels of oxidative stress than wild-type mice (Benigni et al., 2009), suggesting a role for AT(1A)R signaling in the aging process.
Mattson
Mark P
MP
Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov
Maudsley
Stuart
S
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D008136:Longevity; D051379:Mice; D018345:Mice, Knockout; D018384:Oxidative Stress; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000172:deficiency* / Q000235:genetics; D015398:Signal Transduction
D017382:Reactive Oxygen Species; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A