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논문분류	춘계학술대회 초록집
제목	Podocyte-Specific Lysyl Oxidase-Like 2 Deletion Attenuates Diabetic Nephropathy by Suppressing Inflammasome Activation and Fibrosis
저자	Nara Jeon
출판정보	2026; 2026(1):
키워드	podocyte, diabetic nephropathy, lysyl oxidase-like 2 (LOXL2), NLRP3, fibrosis
초록	Objectives: To determine whether podocyte-derived LOXL2 contributes to inflammasome activation and fibrotic remodeling in diabetic nephropathy and to evaluate the impact of podocyte-specific LOXL2 deletion on disease progression. Methods: LOXL2-knockdown (CRISPR/Cas9-mediated) podocytes were exposed to high glucose (HG) and lipopolysaccharide to assess cytoskeletal integrity and inflammasome-related signaling. Podocyte-specific LOXL2-conditional knockout mice (Nphs2-Cre; Loxl2flox/flox) received streptozotocin and a high-fat diet. Albuminuria, podocyte markers, inflammasome activation, inflammatory cell infiltration, and renal fibrosis were evaluated. Results: LOXL2 expression was significantly induced in podocytes under HG and inflammatory stress. LOXL2 deficiency preserved synaptopodin expression and podocyte cytoskeletal organization in vitro and in vivo. LOXL2 suppression significantly attenuated the activation of NOD-like receptor family pyrin domain-containing 3 and Caspase-1, reducing inflammasome priming. In diabetic mice, podocyte-specific LOXL2 deletion caused a marked reduction in albuminuria despite comparable metabolic parameters. Histological analyses demonstrated preserved podocyte number, reduced macrophage infiltration, and significant attenuation of fibrotic remodeling, as evidenced by decreased α-smooth muscle actin accumulation. Conclusion: Podocyte-derived LOXL2 promoted cytoskeletal instability, inflammasome priming, and inflammatory-fibrotic remodeling in DN. Targeted inhibition of LOXL2 preserved podocyte integrity and attenuated disease progression, highlighting LOXL2 as a potential therapeutic target linking structural and inflammatory pathways in DN.
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