Ramasamy Akshara, Mohan Chandra
Biomedical Engineering Department, University of Houston, 3517 Cullen Blvd, Room 2027, Houston, TX 77204, USA.
Int J Mol Sci. 2025 Mar 14;26(6):2621. doi: 10.3390/ijms26062621.
Lupus nephritis (LN), a significant complication of systemic lupus erythematosus (SLE), represents a challenging manifestation of the disease. One of the prominent pathophysiologic mechanisms targeting the renal parenchyma is fibrosis, a terminal process resulting in irreversible tissue damage that eventually leads to a decline in renal function and/or end-stage kidney disease (ESKD). Both glomerulosclerosis and interstitial fibrosis emerge as reliable prognostic indicators of renal outcomes. This article reviews the hallmarks of renal fibrosis in lupus nephritis, including the known and putative drivers of fibrogenesis. A better understanding of the cellular and molecular processes driving fibrosis in LN may help inform the development of therapeutic strategies for this disease, as well as the identification of individuals at higher risk of developing ESKD.
狼疮性肾炎（LN）是系统性红斑狼疮（SLE）的一种重要并发症，是该疾病具有挑战性的一种表现形式。针对肾实质的突出病理生理机制之一是纤维化，这是一个终末期过程，会导致不可逆的组织损伤，最终导致肾功能下降和/或终末期肾病（ESKD）。肾小球硬化和间质纤维化均已成为肾脏预后的可靠预测指标。本文综述了狼疮性肾炎中肾纤维化的特征，包括已知的和推测的纤维化驱动因素。更好地了解驱动LN纤维化的细胞和分子过程，可能有助于为该疾病治疗策略的制定提供依据，并有助于识别发生ESKD风险较高的个体。
