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The mechanisms behind this decline are not fully understood. While excessive production of endothelin 1 (ET-1), a potent vasoconstrictor, is linked to many diseases that increase with age, the role of ET-1 and its receptors in axon regeneration is unknown. Using single cell RNA sequencing, we show that satellite glial cells (SGCs), which completely envelop the sensory neuron soma residing in the dorsal root ganglia (DRG), express the endothelin B receptor (ETBR), while ET-1 is expressed by endothelial cells. Inhibition of ETBR\n                  <jats:italic>ex-vivo<\/jats:italic>\n                  in DRG explant cultures improves axon growth in both adult and aged conditions\n                  <jats:italic>. In vivo,<\/jats:italic>\n                  treatment with the FDA-approved compound, Bosentan, improves axon regeneration and reverses the age-dependent decrease in axonal regenerative capacity. Single-nuclei RNA sequencing and electron microscopy analyses reveal a decreased abundance of SGCs in aged mice compared to adult mice. Additionally, the decreased expression of connexin 43 (Cx43) in SGCs in aged mice after nerve injury is partially rescued by Bosentan treatment. These results reveal that inhibiting ETBR function enhances axon regeneration and rescues the age-dependent decrease in axonal regenerative capacity, providing a potential avenue for future therapies.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>One Sentence Summary<\/jats:title>\n                  <jats:p>Inhibition of endothelin signaling improves nerve regeneration after central and peripheral injuries and counters age-related regenerative decline.<\/jats:p>\n                <\/jats:sec>","DOI":"10.1101\/2024.06.08.597928","type":"posted-content","created":{"date-parts":[[2024,6,10]],"date-time":"2024-06-10T14:05:20Z","timestamp":1718028320000},"source":"Crossref","is-referenced-by-count":0,"title":["Endothelin B receptor inhibition rescues aging-dependent neuronal regenerative decline"],"prefix":"10.64898","author":[{"given":"Rui","family":"Feng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah F.","family":"Rosen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irshad","family":"Ansari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"John","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B.","family":"Thomsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oshri","family":"Avraham","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7671-147X","authenticated-orcid":false,"given":"Cedric G.","family":"Geoffroy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9978-050X","authenticated-orcid":false,"given":"Valeria","family":"Cavalli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2025061109150828000_2024.06.08.597928v3.1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4886(89)90145-3"},{"key":"2025061109150828000_2024.06.08.597928v3.2","doi-asserted-by":"crossref","unstructured":"Andrews, M.R. , S. 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