For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
3
views
105
references
 Top references
cited by
20
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      459
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effects of GH/IGF on the Aging Mitochondria

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The mitochondria are key organelles regulating vital processes in the eukaryote cell. A decline in mitochondrial function is one of the hallmarks of aging. Growth hormone (GH) and the insulin-like growth factor-1 (IGF-1) are somatotropic hormones that regulate cellular homeostasis and play significant roles in cell differentiation, function, and survival. In mammals, these hormones peak during puberty and decline gradually during adulthood and aging. Here, we review the evidence that GH and IGF-1 regulate mitochondrial mass and function and contribute to specific processes of cellular aging. Specifically, we discuss the contribution of GH and IGF-1 to mitochondrial biogenesis, respiration and ATP production, oxidative stress, senescence, and apoptosis. Particular emphasis was placed on how these pathways intersect during aging.

          Related collections

          Most cited references105

          • Record: found
          • Abstract: found
          • Article: not found

          Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion

          Francis Rodier, Jean-Philippe Coppe, Christopher K Patil … (2009)
          Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells1. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments2. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs), which initiate increased secretion of inflammatory cytokines such as interleukin-6 (IL-6). Cytokine secretion occurred only after establishment of persistent DNA damage signaling, usually associated with senescence, not after transient DNA damage responses (DDR). Initiation and maintenance of this cytokine response required the DDR proteins ATM, NBS1 and CHK2, but not the cell cycle arrest enforcers p53 and pRb. ATM was also essential for IL-6 secretion during oncogene-induced senescence and by damaged cells that bypass senescence. Further, DDR activity and IL-6 were elevated in human cancers, and ATM-depletion suppressed the ability of senescent cells to stimulate IL-6-dependent cancer cell invasiveness. Thus, in addition to orchestrating cell cycle checkpoints and DNA repair, a novel and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue.
          Article 0 comments Cited 751 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.

            J Yang, X. Liu, K. Bhalla … (1997)
            Bcl-2 is an integral membrane protein located mainly on the outer membrane of mitochondria. Overexpression of Bcl-2 prevents cells from undergoing apoptosis in response to a variety of stimuli. Cytosolic cytochrome c is necessary for the initiation of the apoptotic program, suggesting a possible connection between Bcl-2 and cytochrome c, which is normally located in the mitochondrial intermembrane space. Cells undergoing apoptosis were found to have an elevation of cytochrome c in the cytosol and a corresponding decrease in the mitochondria. Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria.
            Article 0 comments Cited 610 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans.

              K. D. Kimura, H. A. Tissenbaum, Y. Liu … (1997)
              A C. elegans neurosecretory signaling system regulates whether animals enter the reproductive life cycle or arrest development at the long-lived dauer diapause stage. daf-2, a key gene in the genetic pathway that mediates this endocrine signaling, encodes an insulin receptor family member. Decreases in DAF-2 signaling induce metabolic and developmental changes, as in mammalian metabolic control by the insulin receptor. Decreased DAF-2 signaling also causes an increase in life-span. Life-span regulation by insulin-like metabolic control is analogous to mammalian longevity enhancement induced by caloric restriction, suggesting a general link between metabolism, diapause, and longevity.
              Article 0 comments Cited 481 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 02 June 2020
                Publication date Collection: June 2020
                Volume: 9
                Issue: 6
                Electronic Location Identifier: 1384
                Affiliations
                [1 ]David B. Kriser Dental Center, Department of Molecular Pathobiology, New York University College of Dentistry New York, NY 10010–4086, USA; sbp4@ 123456nyu.edu (S.B.P.); dixitm01@ 123456nyu.edu (M.D.); mn2452@ 123456nyu.edu (M.N.); ep37@ 123456nyu.edu (E.P.)
                [2 ]Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel; mailkartz@ 123456gmail.com (K.N.); hwerner@ 123456tauex.tau.ac.il (H.W.)
                Author notes
                [* ]Correspondence: sy1007@ 123456nyu.edu ; Tel.: +212-998-9721
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-3733-4648
                https://orcid.org/0000-0003-0154-1290
                https://orcid.org/0000-0002-2352-1330
                Article
                Publisher ID: cells-09-01384
                DOI: 10.3390/cells9061384
                PMC ID: 7349719
                PubMed ID: 32498386
                SO-VID: 86b2e816-fa61-49ae-aad9-47cedd98a583
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 16 April 2020
                Date accepted : 26 May 2020
                Categories
                Subject: Review

                Keywords: mitochondria,growth hormone,insulin-like growth factor-1,aging,oxidative stress,senescence
                Data availability:
                Keywords: mitochondria, growth hormone, insulin-like growth factor-1, aging, oxidative stress, senescence

                Comments

                Comment on this article

                scite_

                Similar content459

                See all similar

                Cited by20

                See all cited by

                Most referenced authors2,244

                See all reference authors