Manikandan Subramanian: In Our Latest Study We Uncover a Key Mechanism Behind Clearance of Dying Cells Failure
Manikandan Subramanian, Group Leader and Deputy Director of Research at the William Harvey Research Institute, Barts and The London School of Medicine, shared a post on LinkedIn:
“Clearance of dying cells—lovingly called efferocytosis—is a vital housekeeping role carried out by macrophages. But when this process fails, tissues buckle under pressure of mounting debris and start to dysfunction. In diseases like atherosclerosis, this breakdown can ultimately trigger heart attacks and strokes.
In our latest study, published in Circulation Research and led by Aarushi Singhal we uncover a key mechanism behind this failure. We found that endoplasmic reticulum stress activates the protein TRIB3, which then blocks macrophages from forming the membrane structures needed to engulf and clear dead cells.
In other words, TRIB3 acts as a brake on efferocytosis in atherosclerotic plaques—and targeting it could open new therapeutic pathways for cardiovascular disease.
Title: TRIB3 Links Endoplasmic Reticulum Stress to Impaired Efferocytosis in Atherosclerosis
Authors: Aarushi Singhal, Stefan Russo, Umesh Kumar Dhawan, Kunzangla Bhutia, Christopher G. Bell, Hedayatullah Hayat, Thomas D. Nightingale, Monica de Gaetano, Orina Belton, Eoin Brennan, Patricia B. Munroe, Catherine Godson, Mary Barry, Carol C. Shoulders, Heather L. Wilson, Guillermo Velasco, Endre Kiss-Toth, Manikandan Subramanian
Curious to learn more? Read the full paper here.
A huge thanks to Barts Charity and the British Heart Foundation for supporting this work, and to all our fantastic collaborators who made this possible.”
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