{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T02:25:29Z","timestamp":1791685529346,"version":"4.3.4"},"reference-count":221,"publisher":"MDPI AG","issue":"13","license":[{"start":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T00:00:00Z","timestamp":1750809600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Narodowe Centrum Nauki (Poland)","award":["2021\/43\/B\/NZ4\/01135"],"award-info":[{"award-number":["2021\/43\/B\/NZ4\/01135"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Adenylyl cyclases (ACs) are key regulators of cyclic adenosine monophosphate (cAMP) signaling\u2014a pathway critical for neuroregeneration, synaptic plasticity, and neuronal survival. In both the central and peripheral nervous systems, injury-induced activation of ACs promotes axonal outgrowth and functional recovery through the stimulation of protein kinase A (PKA), exchange proteins directly activated by cAMP (Epac), and cAMP-response element-binding protein (CREB). Among the various AC isoforms, calcium-sensitive AC1, AC8, and AC5, as well as bicarbonate-responsive soluble AC (sAC), have emerged as crucial mediators of neuroplasticity and axon regeneration. These isoforms coordinate diverse cellular responses\u2014including gene transcription, cytoskeletal remodeling, and neurotransmitter release\u2014to metabolic, synaptic, and injury-related signals. Dysregulation of AC activity has been implicated in the pathophysiology of neurodegenerative diseases such as Parkinson\u2019s disease, Alzheimer\u2019s disease, and amyotrophic lateral sclerosis, as well as in chronic pain syndromes. Pharmacological modulation of cAMP levels through AC activation, phosphodiesterase (PDE) inhibition, or pituitary adenylyl cyclase-activating polypeptide (PACAP) receptor signaling has shown therapeutic promise in preclinical models by enhancing neurogenesis, remyelination, and synaptic repair. Conversely, targeted inhibition of specific AC isoforms, particularly AC1, has demonstrated efficacy in reducing maladaptive plasticity and neuropathic pain. This review highlights the diverse roles of ACs in neuronal function and injury response and discusses emerging strategies for their therapeutic targeting.<\/jats:p>","DOI":"10.3390\/ijms26136081","type":"journal-article","created":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T03:53:02Z","timestamp":1750823582000},"page":"6081","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Adenylyl Cyclases as Therapeutic Targets in Neuroregeneration"],"prefix":"10.3390","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-3075-8675","authenticated-orcid":false,"given":"Julia","family":"Tomczak","sequence":"first","affiliation":[{"name":"Department of Molecular Neurochemistry, Faculty of Health Sciences, Medical University of Lodz, 92215 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnieszka","family":"Kapsa","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurochemistry, Faculty of Health Sciences, Medical University of Lodz, 92215 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7654-9011","authenticated-orcid":false,"given":"Tomasz","family":"Boczek","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurochemistry, Faculty of Health Sciences, Medical University of Lodz, 92215 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,6,25]]},"reference":[{"key":"ref_1","first-page":"30","article-title":"Neuroregeneration and Plasticity: A Review of the Physiological Mechanisms for Achieving Functional Recovery Postinjury","volume":"7","author":"Nagappan","year":"2020","journal-title":"Mil. 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