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Cold and hot fibrosis define clinically distinct cardiac pathologies

ABSTRACT: Cold and hot fibrosis define clinically distinct cardiac pathologies

PROVIDER: PRJNA1049432 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27117384_1.fastq.gz	Fastqsanger.gz
	SRR27117384_2.fastq.gz	Fastqsanger.gz
	SRR27117385_1.fastq.gz	Fastqsanger.gz
	SRR27117385_2.fastq.gz	Fastqsanger.gz
	SRR27117386_1.fastq.gz	Fastqsanger.gz

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Cold and hot fibrosis define clinically distinct cardiac pathologies

Project description:Cold and hot fibrosis define clinically distinct cardiac pathologies

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Cold and hot fibrosis define clinically distinct cardiac pathologies

Project description:Fibrosis is a pathology of excessive scarring and a major unmet medical need. Identifying key simplifying principles is needed to better understand fibrosis and may yield new therapeutic approaches. Fibrosis is driven by myofibroblasts that interact with macrophages. We developed a cell-circuit model that predicted two types of fibrosis - ‘hot fibrosis’ that includes both macrophages and myofibroblasts, and ‘cold fibrosis’ dominated by myofibroblasts alone. Here, we tested these concepts using an in-vivo pathological model for cardiac fibrosis resulting from myocardial infarction (MI). We show that MI progresses into cold fibrosis in both mice and pigs. We used the cell-circuit model to find a fragility of cold fibrosis - the autocrine loop which supports myofibroblast growth. We identified the growth factors in the autocrine loop and demonstrate that one of these factors- TIMP1- can stimulate cardiac myofibroblast proliferation in vitro. Inhibiting TIMP1 in-vivo reduced fibrosis in adult mice after MI. This study demonstrates the concept of cold fibrosis following acute MI and the feasibility of our circuit-to-target approach to better understand and treat fibrosis.

2025-02-18 | GSE247856 | GEO

Cold and hot fibrosis define clinically distinct cardiac pathologies

Project description:Fibrosis is a broad pathology of excessive scarring with substantial medical implications. The fibrotic scar is produced by myofibroblasts that interact with macrophages. Fibrosis is a complex process involving thousands of factors, therefore, to better understand fibrosis and develop new therapeutic approaches, it is necessary to simplify and clarify the underlying concepts. Recently, we described a mathematical model for a macrophage-myofibroblast cell circuit, predicting two types of fibrosis - hot fibrosis with abundant macrophages and myofibroblasts, and cold fibrosis dominated by myofibroblasts alone. To test these concepts and intervention strategies in a medically relevant system, we use a widely studied in-vivo injury model for fibrosis, myocardial infarction (MI). We show that cold fibrosis is the final outcome of MI in both mice and pigs and demonstrate that fibrosis can shift toward healing in regenerative settings. MI begind with an increase of myofibroblasts and macrophages, followed by macrophage decline leading to persistent cold fibrosis (only myofibroblasts). During this process, fibroblasts, unlike macrophages, acquire distinct fate changes. Using mathematical modeling we predict that targeting of the autocrine signal for myofibroblast division could block cold fibrosis. We identify TIMP1 as an autocrine cardiac myofibroblast growth factor in-vitro. Treatment of adult mice after MI with anti-TIMP1 antibodies reduces fibrosis in-vivo. This study shows the utility of the concepts of hot and cold fibrosis and the feasibility of our circuit-to-target approach to reduce fibrosis after acute cardiac injury by inhibiting the myofibroblast autocrine loop.

2025-02-18 | GSE249517 | GEO

Cold and hot fibrosis define clinically distinct cardiac pathologies.

Project description:Fibrosis remains a major unmet medical need. Simplifying principles are needed to better understand fibrosis and to yield new therapeutic approaches. Fibrosis is driven by myofibroblasts that interact with macrophages. A mathematical cell-circuit model predicts two types of fibrosis: hot fibrosis driven by macrophages and myofibroblasts and cold fibrosis driven by myofibroblasts alone. Testing these concepts in cardiac fibrosis resulting from myocardial infarction (MI) and heart failure (HF), we revealed that acute MI leads to cold fibrosis whereas chronic injury (HF) leads to hot fibrosis. MI-driven cold fibrosis is conserved in pigs and humans. We computationally identified a vulnerability of cold fibrosis: the myofibroblast autocrine growth factor loop. Inhibiting this loop by targeting TIMP1 with neutralizing antibodies reduced myofibroblast proliferation and fibrosis post-MI in mice. Our study demonstrates the utility of the concepts of hot and cold fibrosis and the feasibility of a circuit-to-target approach to pinpoint a treatment strategy that reduces fibrosis. A record of this paper's transparent peer review process is included in the supplemental information.

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Differentiation-related epigenomic changes define clinically distinct keratinocyte cancer subclasses [methylation]

Project description:Differentiation-related epigenomic changes define clinically distinct keratinocyte cancer subclasses [methylation]

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Differentiation-related epigenomic changes define clinically distinct keratinocyte cancer subclasses [Multiome]

Project description:Differentiation-related epigenomic changes define clinically distinct keratinocyte cancer subclasses [Multiome]

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Project description:Differentiation-related epigenomic changes define clinically distinct keratinocyte cancer subclasses [scRNA-seq]

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Brown-fat-mediated tumour suppression by cold-altered global metabolism

Project description:<p>Glucose uptake is essential for cancer glycolysis and is involved in non-shivering thermogenesis of adipose tissues. Most cancers use glycolysis to harness energy for their infinite growth, invasion and metastasis. Activation of thermogenic metabolism in brown adipose tissue (BAT) by cold and drugs instigates blood glucose uptake in adipocytes. However, the functional effects of the global metabolic changes associated with BAT activation on tumour growth are unclear. Here we show that exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers. Mechanistically, cold-induced BAT activation substantially decreases blood glucose and impedes the glycolysis-based metabolism in cancer cells. The removal of BAT and feeding on a high-glucose diet under cold exposure restore tumour growth, and genetic deletion of Ucp1-the key mediator for BAT-thermogenesis-ablates the cold-triggered anticancer effect. In a pilot human study, mild cold exposure activates a substantial amount of BAT in both healthy humans and a patient with cancer with mitigated glucose uptake in the tumour tissue. These findings provide a previously undescribed concept and paradigm for cancer therapy that uses a simple and effective approach. We anticipate that cold exposure and activation of BAT through any other approach, such as drugs and devices either alone or in combination with other anticancer therapeutics, will provide a general approach for the effective treatment of various cancers.</p>

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The rcf1-1 mutation affects global gene expression in Arabidopsis thaliana with or without cold stress.

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