The Yin and Yang of cellular senescence in ischemia-induced myocardial injury

Rosalie Wolff von Gudenberg; Jasper Iske; Tobias Roeschl; Philipp Stawowy; James L Kirkland; Arjang Ruhparwar; Stefan G Tullius

doi:10.1016/j.tcm.2025.12.004

The Yin and Yang of cellular senescence in ischemia-induced myocardial injury

Trends Cardiovasc Med. 2026 Jul;36(5):281-292. doi: 10.1016/j.tcm.2025.12.004. Epub 2025 Dec 19.

Authors

Rosalie Wolff von Gudenberg¹, Jasper Iske², Tobias Roeschl³, Philipp Stawowy³, James L Kirkland⁴, Arjang Ruhparwar⁵, Stefan G Tullius⁶

Affiliations

¹ Division of Transplant Surgery, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA; Department of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Carl-Neuberg Straße 1, 30625 Hannover, Germany.
² Department of Cardiothoracic and Vascular Surgery, Deutsches Herzzentrum der Charité (DHZC), Augustenburger Platz 1, 13353 Berlin, Germany; Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Charitéplatz 1, 10117 Berlin, Germany.
³ Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Charitéplatz 1, 10117 Berlin, Germany; Department of Cardiology, German Heart Center Berlin, Mittlallee 11,13353 Berlin, Germany.
⁴ Center for Advanced Gerotherapeutics, Department of Medicine, Cedars-Sinai Health Sciences University, Pacific Design Center, 8687 Melrose Avenue, West Hollywood, CA 90069, USA.
⁵ Department of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Carl-Neuberg Straße 1, 30625 Hannover, Germany.
⁶ Division of Transplant Surgery, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. Electronic address: stullius@bwh.harvard.edu.

Abstract

Cellular senescence is a stress responsive program that critically affects chronological and biological aging, ischemia reperfusion injury (IRI), and age related cardiovascular diseases. Of relevance, cardiac senescent cells exhibit altered characteristics that promote inflammation, remodeling, and fibrosis, ultimately contributing to the functional decline following myocardial infarction (MI). At the same time, emerging evidence suggests that senescence may also exert protective effects post-MI, limiting fibrosis. Thus, understanding the mechanisms and pathways of cardiac senescence appears critical for delineating the consequences of IRI, including identification of novel therapeutic targets for improving post-MI recovery.

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