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Given the considerable translation potential, two major strategies have emerged: supplementation of exogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S and modulation of endogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S metabolism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Advances:<\/jats:title>\n                    <jats:p>\n                      Recently, it was reported that hepatic H\n                      <jats:sub>2<\/jats:sub>\n                      S production capacity is increased in two of the best-characterized mammalian models of life span extension, dietary restriction, and hypopituitary dwarfism, leading to new insights into dietary and hormonal regulation of endogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S production together with broader changes in sulfur amino acid (SAA) metabolism with implications for DNA methylation and redox status.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Critical Issues:<\/jats:title>\n                    <jats:p>\n                      Here, we discuss the role of dietary SAAs and growth hormone (GH)\/thyroid hormone (TH) signaling in regulation of endogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S production largely\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      repression of H\n                      <jats:sub>2<\/jats:sub>\n                      S generating enzymes cystathionine \u03b3-lyase (CGL) and cystathionine \u03b2-synthase (CBS) on the level of gene transcription, as well as reciprocal regulation of GH and TH signaling by H\n                      <jats:sub>2<\/jats:sub>\n                      S itself. We also discuss plasticity of CGL and CBS gene expression in response to environmental stimuli and the potential of the microbiome to impact overall H\n                      <jats:sub>2<\/jats:sub>\n                      S levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Future Directions:<\/jats:title>\n                    <jats:p>\n                      The relative contribution of increased H\n                      <jats:sub>2<\/jats:sub>\n                      S to health span or lifespan benefits in models of extended longevity remains to be determined, as does the mechanism by which such benefits occur. Nonetheless, our ability to control H\n                      <jats:sub>2<\/jats:sub>\n                      S levels using exogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S donors or by modifying the endogenous H\n                      <jats:sub>2<\/jats:sub>\n                      S production\/consumption equilibrium has the potential to improve health and increase \u201cshelf-life\u201d across evolutionary boundaries, including our own.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      28, 1483\u20131502.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2017.7434","type":"journal-article","created":{"date-parts":[[2018,3,29]],"date-time":"2018-03-29T11:42:53Z","timestamp":1522323773000},"page":"1483-1502","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":62,"title":["Dietary and Endocrine Regulation of Endogenous Hydrogen Sulfide Production: Implications for Longevity"],"prefix":"10.1177","volume":"28","author":[{"given":"Christopher","family":"Hine","sequence":"first","affiliation":[{"name":"Cleveland Clinic Lerner Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Zhu","sequence":"additional","affiliation":[{"name":"Beth Israel Deaconess Medical Center and Harvard Medical School"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony N.","family":"Hollenberg","sequence":"additional","affiliation":[{"name":"Beth Israel Deaconess Medical Center and Harvard Medical School"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James R.","family":"Mitchell","sequence":"additional","affiliation":[{"name":"Harvard T.H. 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