Open AccessLessons from Cancer Metabolism for Pulmonary Arterial Hypertension and Fibrosis
Author(s) -
Sae Hwang Han,
Navdeep S. Chandel
Publication year - 2021
Publication title -
american journal of respiratory cell and molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.469
H-Index - 161
eISSN - 1535-4989
pISSN - 1044-1549
DOI - 10.1165/rcmb.2020-0550tr
Subject(s) - anabolism , cell metabolism , catabolism , signal transduction , biology , pathogenesis , metabolism , cancer , pulmonary fibrosis , metabolic pathway , cell , cellular metabolism , pulmonary hypertension , bioinformatics , cancer cell , cancer research , fibrosis , microbiology and biotechnology , medicine , immunology , endocrinology , biochemistry , genetics
Metabolism is essential for a living organism to sustain life. It provides energy to a cell by breaking down compounds (catabolism) and supplies building blocks for the synthesis of macromolecules (anabolism). Signal transduction pathways tightly regulate mammalian cellular metabolism. Simultaneously, metabolism itself serves as a signaling pathway to control many cellular processes, such as proliferation, differentiation, cell death, gene expression, and adaptation to stress. Considerable progress in the metabolism field has come from understanding how cancer cells co-opt metabolic pathways for growth and survival. Recent data also show that several metabolic pathways may participate in the pathogenesis of lung diseases, some of which could be promising therapeutic targets. In this translational review, we will outline the basic metabolic principles learned from the cancer metabolism field as they apply to the pathogenesis of pulmonary arterial hypertension and fibrosis and will place an emphasis on therapeutic potential.