Somatic NAP1L1 p.D349E promotes cardiac hypertrophy through cGAS-STING-IFN signaling DOI Creative Commons

Cheng Lv,

Xiayidan Alimu,

Xiao Xiao

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: April 1, 2025

Language: Английский

Pervasive nuclear envelope ruptures precede ECM signaling and disease onset without activating cGAS-STING in Lamin-cardiomyopathy mice DOI Creative Commons

Atsuki En,

Hanumakumar Bogireddi,

Briana Thomas

et al.

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

9

Metrnl and Cardiomyopathies: From Molecular Mechanisms to Therapeutic Insights DOI Creative Commons

Miaomiao Xu,

Xiaoguang Liu, Liming Lu

et al.

Journal 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

1

Heart of the matter: mitochondrial dynamics and genome alterations in cardiac aging DOI Creative Commons
Claudie Gabillard-Lefort,

Théophile Thibault,

Guy Lenaers

et al.

Mechanisms of Ageing and Development, Journal Year: 2025, Volume and Issue: 224, P. 112044 - 112044

Published: Feb. 27, 2025

Language: Английский

Citations

1

Metabolic diseases and interferon immune responses DOI Creative Commons
Haiyan Zhou, Chunyan Liu, Yuerong Zhang

et al.

Deleted 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

1

Somatic NAP1L1 p.D349E promotes cardiac hypertrophy through cGAS-STING-IFN signaling DOI Creative Commons

Cheng Lv,

Xiayidan Alimu,

Xiao Xiao

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: April 1, 2025

Language: Английский

Citations

1