Proposed pathophysiological crosstalk between MAFLD and CKD.

<p>This schematic illustrates the proposed pathophysiological crosstalk between Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Chronic Kidney Disease (CKD). <b>Panel A depicts organ-specific mechanisms:</b> in the <i>liver</i>, steatosis (lipid-laden h...

সম্পূর্ণ বিবরণ

সংরক্ষণ করুন:
গ্রন্থ-পঞ্জীর বিবরন
প্রধান লেখক: Zienab M. Saad (22676502) (author)
অন্যান্য লেখক: Hesham K. H. Keryakos (22676505) (author), Hala A. Hassanin (22676508) (author), Mahmoud M. Higazi (22676511) (author), Manar M. Sayed (22676514) (author), Doaa E. Ismail (22676517) (author), Safaa M. Abdelhalim (21398199) (author)
প্রকাশিত: 2025
বিষয়গুলি:
ট্যাগগুলো: ট্যাগ যুক্ত করুন
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বিবরন
সংক্ষিপ্ত:<p>This schematic illustrates the proposed pathophysiological crosstalk between Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Chronic Kidney Disease (CKD). <b>Panel A depicts organ-specific mechanisms:</b> in the <i>liver</i>, steatosis (lipid-laden hepatocytes) progresses through inflammation (Kupffer cell activation, TNF-α/IL-6 release) to fibrosis (stellate cell activation, collagen deposition); in the <i>kidney</i>, lipotoxicity (podocyte fatty acid influx) leads to podocyte injury (effacement, apoptosis) and glomerulosclerosis (collagen IV accumulation). <b>Panel B highlights systemic mediators</b>: insulin resistance (hyperinsulinemia-driven hepatic gluconeogenesis and renal sodium retention), dyslipidemia (VLDL/ApoB glomerular deposition), and key mediators (fetuin-A, adiponectin deficiency, uric acid-induced NLRP3 activation). Bidirectional interactions amplify organ damage through direct (lipotoxicity, fibrosis) and systemic (metabolic, inflammatory) pathways, suggesting shared therapeutic targets for dual hepatic-renal protection.</p>