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Cited by 8 publications
(8 citation statements)
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References 8 publications
(8 reference statements)
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“…In terms of cardiac aging, mice in which the Atg5 protein is cardiac-specifically deleted through constitutive αMHC-Cre expression develop dilated cardiomyopathy with severe systolic dysfunction during aging, accompanied by sarcomeric disarray and accumulation of dysfunctional and abnormal mitochondria 96 . Cardiac-specific deletion of GSK-3α also promoted the development of cardiac aging, and this was accompanied by suppression of autophagy 120 . One cautionary note is that the use of αMHC-Cre, originally generated by Dr. Michael Schneider’s laboratory for use in aging studies, may potentially be problematic since cardiac-specific Cre alone induces significant time-dependent cardiac dysfunction 121 .…”
Section: The Role Of Autophagy During Aging Of the Heartmentioning
confidence: 97%
“…In terms of cardiac aging, mice in which the Atg5 protein is cardiac-specifically deleted through constitutive αMHC-Cre expression develop dilated cardiomyopathy with severe systolic dysfunction during aging, accompanied by sarcomeric disarray and accumulation of dysfunctional and abnormal mitochondria 96 . Cardiac-specific deletion of GSK-3α also promoted the development of cardiac aging, and this was accompanied by suppression of autophagy 120 . One cautionary note is that the use of αMHC-Cre, originally generated by Dr. Michael Schneider’s laboratory for use in aging studies, may potentially be problematic since cardiac-specific Cre alone induces significant time-dependent cardiac dysfunction 121 .…”
Section: The Role Of Autophagy During Aging Of the Heartmentioning
confidence: 97%
“…GSK-3 is a constitutively active protein kinase that has broad regulatory influence due to the multiplicity of substrates that it can phosphorylate. These substrates include metabolic enzymes, signaling molecules, structural proteins and transcription factors, typically involved in regulating cell proliferation and differentiation, cellular metabolism, cell survival and cell cycle regulation[82,84]. Evidence suggests that GSK-3 is a novel regulator of aging that retards age-related pathologies in a wide variety of tissues[85].…”
Section: Pulmonary Responsementioning
confidence: 99%
“…Cardiomyocytes show age-related changes in the proteostasis pathways, resulting in calcium homeostasis impairment, reactive oxygen species induction, hypertrophy and fibrosis, and eventual structure damage and diminished cardiac function (Klionsky et al, 2016;. Cardiomyocyte-specific deletion of GSK-3a in mice accelerated cardiac aging and reduced basal autophagy levels (Zhou and Force, 2013;. Impaired autophagy with age slows the turnover of damaged proteasomes and contribute to ageassociated CVDs and cardiomyocyte senescence (Korolchuk et al, 2009).…”
Section: Autophagy Regulation and Dysregulation In Cvdmentioning
confidence: 99%