Sirtuin 3–dependent mitochondrial dynamic improvements protect against acute kidney injury

Morigi, Marina; Perico, Luca; Rota, Cinzia; Longaretti, Lorena; Conti, Sara; Rottoli, Daniela; Novelli, Rubina; Remuzzi, Giuseppe; Benigni, Ariela

doi:10.1172/jci77632

Cited by 333 publications

(336 citation statements)

References 34 publications

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“…The biological relevance of SIRT3 as a protective agent against acute tissue damage was also offered by findings in acute kidney injury (AKI) [23]. AKI is a disease characterized by the rapid decrease of renal function, tubular injury, and a high mortality rate [24].…”

Section: Sirt3 and Renal Injurymentioning

confidence: 99%

Mitochondrial Sirtuin 3 and Renal Diseases

Perico

Morigi

Benigni³

2016

Nephron

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Mitochondria are dynamic organelles whose functions are tightly regulated at multiple levels to maintain proper cellular homeostasis. Mitochondrial Sirtuin 3 (SIRT3), which belongs to an evolutionary conserved family of NAD⁺-dependent deacetylases, is a key regulator of the mitochondrial respiratory chain, ATP production, and fatty acid β-oxidation, and it exerts an antioxidant activity. Changes in SIRT3 expression are critical in the pathophysiology of several diseases, such as metabolic syndrome, diabetes, cancer, and aging. In experimental acute kidney injury (AKI), impairment of renal function and development of tubular injury are associated with SIRT3 reduction and mitochondrial dysfunction in proximal tubuli. SIRT3-deficient mice are more susceptible to AKI and die. Pharmacological manipulations able to increase SIRT3 preserve mitochondrial integrity, markedly limit renal injury, and accelerate functional recovery. This review highlights all the selective rescue mechanisms that point to the key role of SIRT3 as a new therapeutic target for curing renal diseases.

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Section: Sirt3 and Renal Injurymentioning

confidence: 99%

Mitochondrial Sirtuin 3 and Renal Diseases

Perico

Morigi

Benigni³

2016

Nephron

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“…50 We are just beginning to comprehend the relationship between these longevity genes and renal health. More research is needed in all species, but the possibility of therapeutically targeting these pathways to improve renal function is intriguing.…”

Section: Molecular Mechanisms Of Renal Agingmentioning

confidence: 99%

Aging in the Canine Kidney

2015

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Given the irreversible nature of nephron loss, aging of the kidney is of special interest to diagnostic and toxicologic pathologists. There are many similarities among histologic lesions in aged human and canine kidneys, including increased frequency of glomerulosclerosis, interstitial fibrosis, and tubular atrophy. Unfortunately, there are few studies in which renal tissue from aged healthy dogs was adequately examined with advanced diagnostics-namely, transmission electron microscopy and immunofluorescence-so age-associated changes in canine podocytes and glomerular basement membranes are poorly characterized. An age-associated decrease in the glomerular filtration rate in humans and dogs (specifically small breed dogs) has been documented. Although lesions in aged rats and mice differ somewhat from those of aged dogs and humans, the knowledge gained from rodent models is still vital to elucidating the pathogenesis of age-associated renal disease. Many novel molecules implicated in renal aging have been identified through genetically modified rodent models and transcriptomic and proteomic analysis of human kidneys. These molecules represent intriguing therapeutic targets and diagnostic biomarkers. Likewise, influencing critical pathways of cellular aging, such as telomere shortening, cellular senescence, and autophagy, could improve renal function in the elderly.

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“…Kidney tissue, mouse 17,96 . Expression of mitochondrial protein after treatment of AKI by antioxidant 17 .…”

Section: Acute Kidney Injurymentioning

confidence: 99%

“…Expression of mitochondrial protein after treatment of AKI by antioxidant 17 . Protective mechanism of mitochondrial sirtuin 96 .…”

Section: Acute Kidney Injurymentioning

confidence: 99%

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Proteomic approaches to the study of renal mitochondria

Tůma¹,

Kuncová²,

Mareš³

et al. 2016

BIOMED PAP

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Background and Aims. Dysfunction of kidney mitochondria plays a critical role in the pathogenesis of a number of renal diseases. Proteomics represents an untargeted attempt to reveal the remodeling of mitochondrial proteins during disease. Combination of separation methods and mass spectrometry allows identification and quantitative analysis of mitochondrial proteins including protein complexes. The aim of this review is to summarize the methods and applications of proteomics to renal mitochondria. Methods. Using keywords "mitochondria", "kidney", "proteomics", scientific databases (PubMed and Web of knowledge) were searched from 2000 to August 2015 for articles describing methods and applications of proteomics to analysis of mitochondrial proteins in kidney. Included were publications on mitochondrial proteins in kidneys of humans and animal model in health and disease. Results and Conclusion. Proteomics of renal mitochondria has been/is mostly used in diabetes, hypertension, acidosis, nephrotoxicity and renal cancer. Integration of proteomics with other methods for examining protein activity is promising for insight into the role of renal mitochondria in pathological states. Several challenges were identified: selection of appropriate model organism, sensitivity of analytical methods and analysis of mitochondrial proteome in different renal zones/biopsies in the course of various kidney disorders.

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Sirtuin 3–dependent mitochondrial dynamic improvements protect against acute kidney injury

Cited by 333 publications

References 34 publications

Mitochondrial Sirtuin 3 and Renal Diseases

Mitochondrial Sirtuin 3 and Renal Diseases

Aging in the Canine Kidney

Proteomic approaches to the study of renal mitochondria

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