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Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD), and thus, appropriate animal models are critically needed to investigate its pathogenesis and identify new therapeutic targets. DN mouse models are important tools for studying the mechanisms of DN and exploring therapeutic strategies. Common features of the renal pathology in diabetic patients include thickening of the glomerular basement membrane, mesangial expansion, glomerulosclerosis, tubular injury, and interstitial fibrosis. Although DN mouse models generated through pharmacological or genetic approaches demonstrate comparable renal structural changes, the existing DN mouse models fail to replicate the severity of human DN pathology, underscoring the need for further research to develop more precise DN mouse models. Mouse models with renal pathology that better matches the human condition would provide a key platform for identifying potential therapeutic targets and developing new drugs. This review summarizes the advantages and limitations of various DN mouse models, including pharmacological and dietary induction models, genetically engineered models, spontaneous models generated via genetic modification, and models developed by combined modeling approaches. The goal of this review is to provide valuable insights and guidance for the construction of more comprehensive DN models. Not applicable.
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http://dx.doi.org/10.1186/s12882-025-04432-5 | DOI Listing |
Nano Lett
September 2025
State Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
An optimal administration approach is critical for effective mRNA delivery and treatment. Nebulizer inhalation offers a mild, convenient, and noninvasive strategy with high translational potential but primarily focused on lung delivery. In this study, we found that surface charges influence tissue targeting of mRNA lipid nanoparticle (mRNA-LNP) postnebulization.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Rehabilitation Medicine, Second Xiangya Hospital, Central South University, Changsha 410011.
Objectives: Osteoarthritis (OA) is one of the most common chronic degenerative diseases, with chondrocyte apoptosis and extracellular matrix (ECM) degradation as the major pathological changes. The mechanical stimulation can attenuate chondrocyte apoptosis and promote ECM synthesis, but the underlying molecular mechanisms remain unclear. This study aims to investigate the role of primary cilia (PC) in mediating the effects of mechanical stimulation on OA progression.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Pathology, First Clinical College, Changzhi Medical College, Changzhi 046000.
Objectives: Acute lung injury (ALI) is an acute respiratory failure syndrome characterized by impaired gas exchange. Due to the lack of effective targeted drugs, it is associated with high mortality and poor prognosis. (TW) has demonstrated anti-inflammatory activity in the treatment of various diseases.
View Article and Find Full Text PDFClin Mol Hepatol
September 2025
Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Guangzhou, China.
Background/aims: Endoplasmic reticulum (ER) stress in hepatocytes plays a causative role in alcohol-associated liver disease (ALD). The incomplete inhibition of ER stress by targeting canonical ER stress sensor proteins suggests the existence of noncanonical ER stress pathways in ALD pathology. This study aimed to delineate the role of RAB25 in ALD and its regulatory mechanism in noncanonical ER stress pathways.
View Article and Find Full Text PDFBiol Open
September 2025
Departments of Biochemistry & Medical Genetics, University of Manitoba, Winnipeg, R3T 2N2, Canada.
The GM2 gangliosidoses are lysosomal storage disorders exhibiting a spectrum of neurological phenotypes ranging from childhood death to debilitating adult-onset neurological impairment. To date, no mouse model harbouring a specific human mutation causing GM2 gangliosidosis has been created. We used CRISPR/Cas9 to generate knockin (KI) mice with the common adult-onset Hexa Gly269Ser variant as well as knockout (KO) mice with Hexa mutations expected to cause complete HexA deficiency.
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