Cover Story Current Issue

Postpartum (PP) maternal mortality remains alarmingly high, with a rate of 32.9 per 100,000 live births in 2021 in the United States. Cardiovascular diseases, including peripartum/postpartum cardiomyopathy (PPCM) and coronary heart disease, are among the leading causes of PP morbidity and mortality. Although socioeconomic status and the level of PP care can influence the mortality rate, the underlying mechanisms leading to PPCM are not well understood. PPCM is clinically defined as (1) the development of the disease in the last month of pregnancy or within 5 months of delivery, (2) absence of pre-existing heart disease prior to the last month of pregnancy, (3) unknown cause of heart failure, and (4) left ventricular systolic dysfunction. Prognosis remains poor, with full recovery reported in only 23% of affected individuals and 50% experiencing heart failure-related mortality due to limited therapeutic options. Limited studies in both humans and mouse models of PPCM have proposed several potential mechanisms, including inflammation, viral myocarditis, autoimmune reactions, oxidative stress, and apoptosis, resulting from environmental as well as genetic factors. Studying these mechanisms in animal models, particularly those involving genetic causes, has been difficult due to the lack of severity or relevance of existing mouse models of PPCM to the human disease.

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Current Issue

Regulating the cell differentiation trajectory of progenitor cells in adipose tissue fibrosis

Li Zhang, Xinjiang Cai, Xiuju Wu, Zheng Jing, ... Kristina I. Boström

Regulating the cell differentiation trajectory of progenitor cells in adipose tissue fibrosis

 

Objective

Adipose fibrosis signifies pathological remodeling of white adipose tissue (WAT) associated with insulin resistance, diabetes, and cardiovascular disease. Matrix Gla protein (MGP) balances bone morphogenetic protein (BMP) and transforming growth factor β (TGFβ) signaling but has an unclear role in WAT.

Methods

To study the role of MGP in WAT, we used mice with global or platelet-derived growth factor receptor α (Pdgfra)-Cre-mediated Mgp deletion in adipose progenitor cells (APCs) together with single cell RNA sequencing (scRNA-seq), characterization on adipose and fibrotic phenotypes, and BMP and TGFβ signaling studies.

Results

Our results showed that Mgp deletion promotes fibrosis and impairs adipogenesis in mice with global or Pdgfra-Cre-mediated Mgp deletion in APCs. ScRNA-seq showed two new adipose-derived stem cells (ASC) populations, ASC1 and ASC4, emerging after Mgp deletion. Trajectory analysis found that ASC1 and ASC4 were derived from ASC2, which normally undergo adipogenesis but instead had diverted to fibrogenic differentiation. All three ASCs expressed Pdgfra and dipeptidyl peptidase-4 (Dpp4). Inhibition of TGFβ signaling or DPP4 activity in mice with Pdgfra-Cre-mediated Mgp deletion reduced the size of the PDGFRα+; DPP4+ cell population and rescued the WAT from unwanted fibrosis.

Conclusions

MGP is essential for appropriate balance between adipogenic differentiation and fibroblast activation. Dysregulation of PDGFRα+; DPP4+ cells may signal early adipose fibrosis.

 

Articles in Press

Regulating the cell differentiation trajectory of progenitor cells in adipose tissue fibrosis

Li Zhang, Xinjiang Cai, Xiuju Wu, Zheng Jing, ... Kristina I. Boström

Regulating the cell differentiation trajectory of progenitor cells in adipose tissue fibrosis

 

Objective

Adipose fibrosis signifies pathological remodeling of white adipose tissue (WAT) associated with insulin resistance, diabetes, and cardiovascular disease. Matrix Gla protein (MGP) balances bone morphogenetic protein (BMP) and transforming growth factor β (TGFβ) signaling but has an unclear role in WAT.

Methods

To study the role of MGP in WAT, we used mice with global or platelet-derived growth factor receptor α (Pdgfra)-Cre-mediated Mgp deletion in adipose progenitor cells (APCs) together with single cell RNA sequencing (scRNA-seq), characterization on adipose and fibrotic phenotypes, and BMP and TGFβ signaling studies.

Results

Our results showed that Mgp deletion promotes fibrosis and impairs adipogenesis in mice with global or Pdgfra-Cre-mediated Mgp deletion in APCs. ScRNA-seq showed two new adipose-derived stem cells (ASC) populations, ASC1 and ASC4, emerging after Mgp deletion. Trajectory analysis found that ASC1 and ASC4 were derived from ASC2, which normally undergo adipogenesis but instead had diverted to fibrogenic differentiation. All three ASCs expressed Pdgfra and dipeptidyl peptidase-4 (Dpp4). Inhibition of TGFβ signaling or DPP4 activity in mice with Pdgfra-Cre-mediated Mgp deletion reduced the size of the PDGFRα+; DPP4+ cell population and rescued the WAT from unwanted fibrosis.

Conclusions

MGP is essential for appropriate balance between adipogenic differentiation and fibroblast activation. Dysregulation of PDGFRα+; DPP4+ cells may signal early adipose fibrosis.

 

Opening Abstract Submission & Registration

13th
Helmholtz Diabetes Conference 
Munich, 21-23. Sep 2026                                                                                                                             

2024 impact factor: 6.6

You are what you eat

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