2015
DOI: 10.1016/j.yexcr.2015.04.005
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Heme oxygenase-1 enhances autophagy in podocytes as a protective mechanism against high glucose-induced apoptosis

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Cited by 89 publications
(57 citation statements)
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“…demonstrated that impaired podocyte autophagy exacerbates proteinuria in type II diabetic nephropathy models. Similarly, our previous studies also revealed that high glucose (HG) leads to increased autophagy in podocytes at an early stage and that autophagy is a prosurvival mechanism under these conditions16.…”
mentioning
confidence: 57%
“…demonstrated that impaired podocyte autophagy exacerbates proteinuria in type II diabetic nephropathy models. Similarly, our previous studies also revealed that high glucose (HG) leads to increased autophagy in podocytes at an early stage and that autophagy is a prosurvival mechanism under these conditions16.…”
mentioning
confidence: 57%
“…HO-1 activator hemin increased AMPK phosphorylation which in turn, increased markers of autophagy, LC3-II and Beclin-1 expression [51]. In diabetic cardiomyopathic mice, HO-1 overexpression increased AMPK phosphorylation which partially restored cardiac autophagy in diabetic mice [49].…”
Section: Induction Of Autophagy By Ho-1mentioning
confidence: 95%
“…The induction of HO-1 leads to increased cellular CO production, which generates a redox signal for the induction of mitochondrial biogenesis through stimulation of mitochondrial ROS production (5,23). HO-1 has also been implicated in the induction of macroautophagy, (24) and if this capacity includes mitophagy, the enzyme would be involved in the regulation of the entire mitochondrial quality control cycle, which enables accurate and precise mitochondrial turnover (24)(25)(26). Disruption of mitophagy is proinflammatory and prooxidant (27,28), and impaired autophagy compromises bioenergetics and leads to cell death, chronic inflammatory heart disease, and HF progression (29,30).…”
Section: Introductionmentioning
confidence: 99%