PDGFRα inhibition reduces myofibroblast expansion in the fibrotic rim and enhances recovery after ischemic stroke.

Ischemic stroke is a major cause of adult disability. Early treatment with thrombolytics and/or thrombectomy can significantly improve outcomes; however, following these acute interventions, treatment is limited to rehabilitation therapies. Thus, the identification of therapeutic strategies that can help restore brain function in the post-acute phase remains a major challenge.

In situ detection of PD1-PD-L1 interactions as a functional predictor for response to immune checkpoint inhibition in NSCLC.

Background: Immune checkpoint inhibitors (ICIs) have transformed lung cancer treatment, yet their effectiveness appears restricted to certain patient subsets. Current clinical stratification based on PD-L1 expression offers limited predictive value. Given the mechanism of action, directly detecting spatial PD1-PD-L1 interactions might yield more precise insights into immune responses and treatment outcomes.

Different gene expression patterns between mouse and human brain pericytes revealed by single-cell/nucleus RNA sequencing.

Aims: Pericytes in the brain play important roles for microvascular physiology and pathology and are affected in neurological disorders and neurodegenerative diseases. Mouse models are often utilized for pathophysiology studies of the role of pericytes in disease; however, the translatability is unclear as brain pericytes from mouse and human have not been systematically compared. In this study, we investigate the similarities and differences of brain pericyte gene expression between mouse and human.

Thrombolysis exacerbates cerebrovascular injury after ischemic stroke via a VEGF-B dependent effect on adipose lipolysis.

Cerebrovascular injuries leading to edema and hemorrhage after ischemic stroke are common. The mechanisms underlying these events and how they are connected to known risk factors for poor outcome, like obesity and diabetes, is relatively unknown. Herein we demonstrate that increased adipose tissue lipolysis is a dominating risk factor for the development of a compromised cerebrovasculature in ischemic stroke.

Adipose stem cells are sexually dimorphic cells with dual roles as preadipocytes and resident fibroblasts.

Cell identities are defined by intrinsic transcriptional networks and spatio-temporal environmental factors. Here, we explored multiple factors that contribute to the identity of adipose stem cells, including anatomic location, microvascular neighborhood, and sex. Our data suggest that adipose stem cells serve a dual role as adipocyte precursors and fibroblast-like cells that shape the adipose tissue's extracellular matrix in an organotypic manner.