Fine-Tuning of PGC1α Expression Regulates Cardiac Function and Longevity

Published on 2019in Circulation Research15.86
· DOI :10.1161/circresaha.119.315529
Xudong Zhu2
Estimated H-index: 2
(Hangzhou Normal University),
Weiyan Shen (JNU: Jinan University)+ 9 AuthorsZhenyu Ju21
Estimated H-index: 21
(JNU: Jinan University)
Rationale: PGC1α represents an attractive target interfering bioenergetics and mitochondrial homeostasis, yet multiple attempts have failed to upregulate PGC1α expression as a therapy, for instance...
  • References (44)
  • Citations (0)
Published on Nov 1, 2018in Embo Molecular Medicine10.62
Gabriele Civiletto4
Estimated H-index: 4
(University of Cambridge),
Gabriele Civiletto1
Estimated H-index: 1
(University of Cambridge)
+ 6 AuthorsCarlo Viscomi22
Estimated H-index: 22
(University of Cambridge)
Abstract The mTOR inhibitor rapamycin ameliorates the clinical and biochemical phenotype of mouse, worm, and cellular models of mitochondrial disease, via an unclear mechanism. Here, we show that prolonged rapamycin treatment improved motor endurance, corrected morphological abnormalities of muscle, and increased cytochrome c oxidase (COX) activity of a muscle‐specific Cox15 knockout mouse ( Cox15 sm / sm ). Rapamycin treatment restored autophagic flux, which was impaired in naive Cox15 sm / sm ...
Published on Sep 1, 2018in Nature43.07
Danielle A. Sliter11
Estimated H-index: 11
(NIH: National Institutes of Health),
Jennifer Martinez15
Estimated H-index: 15
(NIH: National Institutes of Health)
+ 11 AuthorsDerek P. Narendra14
Estimated H-index: 14
(NIH: National Institutes of Health)
Although serum from patients with Parkinson’s disease contains elevated levels of numerous pro-inflammatory cytokines including IL-6, TNF, IL-1β, and IFNγ, whether inflammation contributes to or is a consequence of neuronal loss remains unknown1. Mutations in parkin, an E3 ubiquitin ligase, and PINK1, a ubiquitin kinase, cause early onset Parkinson’s disease2,3. Both PINK1 and parkin function within the same biochemical pathway and remove damaged mitochondria from cells in culture and in animal ...
Published on Apr 1, 2018in Bulletin of Experimental Biology and Medicine0.57
T. G. Kulikova1
Estimated H-index: 1
O. V. Stepanova1
Estimated H-index: 1
+ 7 AuthorsG. T. Sukhikh20
Estimated H-index: 20
Published on Dec 1, 2017in Nature Medicine30.64
Lingjuan He16
Estimated H-index: 16
Yan Li43
Estimated H-index: 43
+ 24 AuthorsLibo Zhang13
Estimated H-index: 13
Genetic cell-lineage tracing studies in mice are crucial for delineating the contribution of stem and progenitor cells to different cell types, both in disease states and after regenerative therapy. He et al. have developed new genetic lineage-tracing systems that provide more definitive results than the commonly used Cre-based system and show that this new technology can resolve current controversies in the field, as demonstrated by lineage-tracing studies in the heart and liver.
Published on Dec 1, 2017in Nature43.07
Vincenzo Sorrentino16
Estimated H-index: 16
(EPFL: École Polytechnique Fédérale de Lausanne),
Mario Romani2
Estimated H-index: 2
(EPFL: École Polytechnique Fédérale de Lausanne)
+ 9 AuthorsSolène Rietsch1
Estimated H-index: 1
(EPFL: École Polytechnique Fédérale de Lausanne)
Amyloid-β peptide proteopathies disrupt mitochondria, and restoring mitochondrial proteostasis reduces protein aggregation in animal models of amyloid-β disease.
Published on May 1, 2017in Nature43.07
Timothy S. Luongo11
Estimated H-index: 11
(TU: Temple University),
Jonathan P Lambert3
Estimated H-index: 3
(TU: Temple University)
+ 13 AuthorsJop H. van Berlo18
Estimated H-index: 18
Conditional deletion of the mitochondrial Na+/Ca2+ exchanger NCLX in adult mouse hearts causes sudden death due to mitochondrial calcium overload, whereas its overexpression limits cell death elicited by ischaemia reperfusion injury and heart failure.
Published on Apr 3, 2017in Journal of Clinical Investigation12.28
Rick B. Vega11
Estimated H-index: 11
Daniel P. Kelly74
Estimated H-index: 74
Abstract The adult heart is uniquely designed and equipped to provide a continuous supply of energy in the form of ATP to support persistent contractile function. This high-capacity energy transduction system is the result of a remarkable surge in mitochondrial biogenesis and maturation during the fetal-to-adult transition in cardiac development. Substantial evidence indicates that nuclear receptor signaling is integral to dynamic changes in the cardiac mitochondrial phenotype in response to dev...
Published on Dec 1, 2016in Nature Medicine30.64
Tobias Eisenberg36
Estimated H-index: 36
Mahmoud Abdellatif4
Estimated H-index: 4
+ 56 AuthorsAlbrecht Schmidt28
Estimated H-index: 28
Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin ph...
Published on Sep 1, 2016in Nature43.07
Chi Luo5
Estimated H-index: 5
Ji-Hong Lim9
Estimated H-index: 9
+ 5 AuthorsPere Puigserver60
Estimated H-index: 60
Tumour progression is associated with reprogramming of the normal metabolic processes. But do metabolic regulatory circuits affect cancer metastasis? Pere Puigserver and colleagues address this question in melanoma, the deadliest form of skin cancer. They find that PGC1a transcriptional coactivator known to promote biogenesis of mitochondria and to protect against oxidative stresssuppresses melanoma metastasis, through a transcriptional pathway that is parallel to, but distinct from, that leadin...
Published on Jun 1, 2016in Nature Cell Biology17.73
Verónica Torrano7
Estimated H-index: 7
Lorea Valcarcel-Jimenez6
Estimated H-index: 6
+ 34 AuthorsMarc Guiu12
Estimated H-index: 12
Torrano et al. use bioinformatics analyses to identify PGC1α as a transcriptional regulator of a metabolic program downstream of ERRα that opposes metastatic dissemination in prostate cancer.
Cited By0