
Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)
Published: April 1, 2025
Language: Английский
Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)
Published: April 1, 2025
Language: Английский
Cell Reports, Journal Year: 2024, Volume and Issue: 43(6), P. 114284 - 114284
Published: May 29, 2024
Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations Lamin A/C, a nuclear lamina component. Here, we test prevailing hypothesis that NE trigger the pathological cGAS-STING cytosolic DNA-sensing pathway using mouse model of cardiomyopathy. The reduction A/C cardio-myocyte adult mice causes pervasive cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal followed DNA damage accumulation without causing immediate cardiomyocyte death. However, cGAS-STING-dependent signaling remains inactive. Deleting cGas or Sting does not rescue cardiomyopathy model. lack activation is likely due to near absence cGAS expression cardiomyocytes at baseline. Instead, extracellular matrix (ECM) activated predicted initiate pro-inflammatory communication from Lamin-reduced fibroblasts. Our work nominates ECM signaling, cGAS-STING, as potential contributor
Language: Английский
Citations
9Journal of Cellular and Molecular Medicine, Journal Year: 2025, Volume and Issue: 29(2)
Published: Jan. 1, 2025
ABSTRACT Cardiomyopathies, a diverse group of diseases affecting the heart muscle, continue to pose significant clinical challenges due their complex aetiologies and limited treatment options targeting underlying genetic molecular dysregulations. Emerging evidence indicates that Metrnl, myokine, adipokine cardiokine, plays role in pathogenesis various cardiomyopathies. Therefore, objective this review is examine mechanism Metrnl cardiomyopathies, with expectation providing new insights for these diseases.
Language: Английский
Citations
1Mechanisms of Ageing and Development, Journal Year: 2025, Volume and Issue: 224, P. 112044 - 112044
Published: Feb. 27, 2025
Language: Английский
Citations
1Deleted Journal, Journal Year: 2025, Volume and Issue: unknown
Published: March 13, 2025
Abstract Metabolic diseases, including obesity, diabetes, and metabolic‐associated fatty liver disease (MAFLD), are increasingly common worldwide, posing a significant public health challenge. Recent research has revealed complex interplay between these metabolic disorders interferon (IFN) immune responses. As key regulators, interferons coordinate the host's defense against viral infections essential for maintaining homeostasis. However, dysregulation can significantly disrupt IFN signaling pathways, affecting intensity efficiency of Conversely, alterations in influence onset progression diseases. This review explores mechanisms by which diseases modulate responses, focusing on how MAFLD alter signaling. Additionally, we examine implications changes responses By synthesizing current research, this aims to elucidate offering insights future clinical applications field IFN‐related
Language: Английский
Citations
1Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)
Published: April 1, 2025
Language: Английский
Citations
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