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Recent studies have highlighted that key signaling pathways, including Toll-like receptor\/nuclear factor-\u03baB (TLR\/NF-\u03baB), Janus kinase\/signal transducer and activator of transcription (JAK\/STAT), purinergic P2X7 receptor\u2013inflammasome signaling, heat-shock protein\u2013mediated stress responses, and phosphoinositide 3-kinase\/Akt\/mammalian target of rapamycin (PI3K\/Akt\/mTOR) cascades, govern the initiation, amplification, and resolution of ischemic renal injury. These pathways converge on downstream cellular effectors such as cell adhesion molecules (CAMs), which orchestrate leukocyte recruitment, endothelial-epithelial interactions, and spatial propagation of inflammation within the renal microvasculature. Natural compounds have emerged as promising therapeutic candidates for ischemic AKI due to their pleiotropic pharmacological properties and ability to modulate multiple pathogenic signaling networks simultaneously. A growing body of experimental evidence demonstrates that polyphenols, glycosides, saponins, and related phytochemicals attenuate ischemic renal injury by suppressing inflammatory signaling, reducing CAM expression, preserving microcirculatory integrity, and promoting adaptive repair. Furthermore, advances in nanocarrier-based delivery systems have substantially enhanced the translational potential of these compounds by improving bioavailability, renal targeting, and pathway-specific modulation. In this review, we provide a comprehensive, signaling-centered analysis of ischemic AKI pathogenesis and systematically map natural compounds to their molecular targets and downstream inflammatory effectors. By integrating mechanistic insights with emerging nanotherapeutic strategies, this work offers a structured framework for the rational development of multi-target, mechanism-based interventions for ischemic AKI. It highlights key challenges and future directions for clinical translation.<\/jats:p>","DOI":"10.1007\/s12272-026-01601-4","type":"journal-article","created":{"date-parts":[[2026,4,26]],"date-time":"2026-04-26T11:46:28Z","timestamp":1777203988000},"page":"577-635","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Natural compounds targeting inflammatory signaling and cell adhesion molecules in ischemic acute kidney injury"],"prefix":"10.1007","volume":"49","author":[{"given":"Sally A.","family":"Fahim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed M.","family":"El-Dessouki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nada","family":"Osama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sherif S. 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