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Transition from healthy to diseased state is a cell-type-specific process, influenced by neighboring cells and resulting in functionally meaningful differences between pulmonary artery adventitial fibroblasts and smooth muscle cells.

Exogenous mitochondrial transplantation improves cardiac function after cardiopulmonary resuscitation (CPR) may be related to improving mitochondrial function, reducing the oxidative stress response, and decreasing apoptosis in myocardial cells.

The estimation of individual genetic effects across different contexts can be boiled down to a bias-variance trade-off, yet for complex traits, the joint consideration of numerous causal effects alters this trade-off.

The crosstalk between cancerous lesions and the immune system in the lungs demonstrates the complex role of fibroblasts.