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It describes RNA-silencing via CRISPR-Cas13a as selectively targeting harmful long non-coding RNAs, delivered with lipid nanoparticles alongside orally formulated polyphenols. Remaining barriers include targeted delivery, collateral RNA cleavage, immune/toxicity risks, and variability in polyphenol absorption, emphasizing the need for careful translation and clinical 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is renal fibrosis central to chronic kidney disease in this letter?","Question",{"text":63,"@type":64},"The letter states that CKD develops primarily from renal fibrosis and connects it with metabolic-syndrome-like changes, reduced polyphenols, and gut imbalance that worsen inflammation and scarring.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How does CRISPR-Cas13a work in the proposed therapy?",{"text":68,"@type":64},"Cas13a is presented as an RNA-targeting tool that selectively silences harmful long non-coding RNAs without permanently changing DNA, aiming to reduce fibrotic drivers.",{"name":70,"@type":61,"acceptedAnswer":71},"What main barriers limit practical clinical use of Cas13-based renal fibrosis therapies?",{"text":72,"@type":64},"Key challenges include achieving efficient, kidney-specific delivery, minimizing collateral RNA cleavage and unintended targeting, managing immune and toxicity responses, and addressing variability in polyphenol absorption and 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fibrosis  \nKhadija Rameen, MBBSa , Manahil Shoukat, MBBSa , Muhammad Talha, MBBSb , Mahnoor Fatima, MBBSc ,*, Ubaid Ur Rehman, MBBSb  \nTo the Editor,  \nChronic kidney disease (CKD) primarily develops from renal fibrosis, a disease now also visible in individuals displaying symptoms resembling metabolic syndrome. Research and polls have shown that factors including metabolic changes, loss of polyphenols, and intestinal imbalance exacerbate inflammation and kidney scarring[1] . These results point to an evolving connection between nutrition, gut flora, and fibrotic kidney disorders, therefore creating opportunities for fresh treatment options. Regrettably, current drugs have shown somewhat limited ability to stop the development of illnesses. Recent data show that urinary polyphenol metabolites might be good biomarkers for diagnosis and therapy monitoring[2] . This is in line with the TITAN Guidelines on the need for transparency in AI use in healthcare[3] .  \nThis helps to explain how polyphenols might help to lower fibrosis, inflammation, and oxidative stress. Less investigated, the eggplant’s calyx is high in polyphenols and might offer a bright new medicinal source. Using RNA-silencing approaches, nearly a 55% reversal of fibrosis markers was reached in laboratory experiments on kidney organoids utilizing these polyphenols. Already proven in animal models[4], the CRISPR-Cas13a system has the benefit of selectively silencing damaging long non-coding RNAs without permanently changing DNA. Using Cas13a supplied via lipid nanoparticles with orally consumed nano-formulated eggplant polyphenols, a dual-therapy strategy might improve general treatment results. This mix combines a realistic nanomedicine plan with the possibility of greatly enhancing CKD treatment.  \nThe use of Cas13-mediated RNA silencing with natural polyphenols proves to be an innovation for treating renal fibrosis, especially in patients affected by metabolic syndrome. Cas13 is  \naDepartment of Medicine, IBADAT International University, Islamabad, Pakistan, bDepartment of Medicine, King Edward Medical University, Lahore, Pakistan and cDepartment of Medicine, Shaheed Ziaur Rahman Medical College, Rajshahi Medical University, Bogura, Bangladesh  \nSponsorships or competing interests that may be relevant to content are disclosed at the end of this article.  \n*Corresponding author. Address: Shaheed Ziaur Rahman Medical College, Rajshahi Medical University, Ladies hostel, Shaheed Ziaur Rahman Medical College, Bogura 5800, Bangladesh. Tel.: +8801972635581.  \n[E-mail: mahnoorzahid786@gmail.com](E-mail: mahnoorzahid786@gmail.com) (M. Fatima).  \nCopyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc. This isan open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.  \nAnnals of Medicine & Surgery (2026) 88:1120–1121  \nReceived 20 October 2025; Accepted 25 November 2025  \nPublished online 9 December 2025  \n[http://dx.doi.org/10.1097/MS9.0000000000004528](http://dx.doi.org/10.1097/MS9.0000000000004528)  \na flexible RNA-targeting tool that can silence harmful transcripts with accuracy, making it a practical option for future therapies[5] . In nephrology, CRISPR-based methods are already being explored to act on pathways that promote fibrosis, focusing not only on controlling symptoms but also on personalized therapies[6] . When combined, gene silencing and natural compounds may not only target early disease signals but also limit long-term tissue scarring. Together, these interventions provide hope for expanding treatment choices, especially for patients who currently have very limited options.  \nAlthough positive results have been observed, several barriers still limit the practical use of Cas13-based th","cbCaimEOhBMGccFh","https://ap.wps.com/l/cbCaimEOhBMGccFh","pdf",146016,"English","# Background: renal fibrosis and gut-nutrition links\n# Proposed dual-action approach: polyphenols and Cas13a RNA silencing\n# Delivery and translational challenges\n# Comparison with conventional therapy\n# Conclusion","[{\"question\":\"Why is renal fibrosis central to chronic kidney disease in this letter?\",\"answer\":\"The letter states that CKD develops primarily from renal fibrosis and connects it with metabolic-syndrome-like changes, reduced polyphenols, and gut imbalance that worsen inflammation and scarring.\"},{\"question\":\"How does CRISPR-Cas13a work in the proposed therapy?\",\"answer\":\"Cas13a is presented as an RNA-targeting tool that selectively silences harmful long non-coding RNAs without permanently changing DNA, aiming to reduce fibrotic drivers.\"},{\"question\":\"What main barriers limit practical clinical use of Cas13-based renal fibrosis therapies?\",\"answer\":\"Key challenges include achieving efficient, kidney-specific delivery, minimizing collateral RNA cleavage and unintended targeting, managing immune and toxicity responses, and addressing variability in polyphenol absorption and metabolism.\"}]","CRISPR-Cas13 and polyphenol nanotherapy: a dual-action frontier against renal fibrosis - Letter to the Editor | PDF",1790690430]