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Myeloid Cell–Driven Inflammatory Responses Exacerbate Myocardial Cell Injury in Mice

Rajesh Kumar Sharma 1, Anjali Mehta 2, Vivek Reddy Narayan 3, Sneha Patel ORCID

1All India Institute of Medical Sciences (AIIMS) New Delhi, India.
2Postgraduate Institute of Medical Education and Research (PGIMER) Chandigarh, India.
3Department of Internal Medicine, Christian Medical College (CMC).
4Department of Molecular Biology & Biotechnology, Indian Institute of Science (IISc) Bangalore, Karnataka, India.

DOI: 10.18081/2378-5225/15.1  
Cited by 0

 Article history: Received 30 October 2025 · Revised 30 November 2025 · Accepted 12 December 2025 · Published 03 January 2026

© 2026 Patel, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC BY 4.0)

CC BY 4.0                                                                                                   


Abstract

Myocardial cell injury is a central pathological process underlying acute myocardial infarction, ischemia–reperfusion injury, and inflammatory cardiomyopathies. Although ischemic and metabolic disturbances initiate cardiomyocyte damage, accumulating evidence indicates that immune-mediated inflammatory responses significantly amplify myocardial injury. Among immune populations, myeloid cells—including monocytes, macrophages, and neutrophils—play a dominant role in shaping the inflammatory microenvironment of the injured heart. Experimental murine studies have demonstrated that these cells exacerbate myocardial injury through cytokine production, oxidative stress, inflammasome activation, and direct cellular interactions with cardiomyocytes. Importantly, the temporal dynamics and phenotypic heterogeneity of myeloid cells critically determine whether inflammation promotes injury or facilitates repair. This review provides a comprehensive synthesis of the mechanisms by which myeloid cell–driven inflammation worsens myocardial cell injury in mice, with emphasis on molecular signaling pathways, immunometabolic regulation, and translational implications. Understanding these processes offers opportunities for targeted immunomodulatory therapies aimed at preserving myocardial integrity and improving clinical outcomes.

Keywords: Myocardial injury; Myeloid cells; Inflammation; Macrophages; Neutrophils; Cardiomyocyte death; Oxidative stress; Cytokines.


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BM-Publisher · Pathophysiology of Cell Injury Journal (PCIJ) · E-ISSN 2378-5225 · DOI Prefix 10.18081/pcij/2378-5225

Pathophysiology of Cell Injury Journal (PCIJ)
E-ISSN 2378-5225 · Biannual
BM-Publisher (London, UK)
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Vol 15, Issue 1 (January 2026), pp. 1–18

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How to cite (AMA)

Sharma RK, Mehta A, Narayan VR, Patel S. RMyeloid Cell–Driven Inflammatory Responses Exacerbate Myocardial Cell Injury in Mice. Pathophysiology of Cell Injury Journal (PCIJ). 2026;15(1):1–18. doi: 10.18081/2378-5225/15.1.

More citation

Rajesh Kumar Sharma, A. M. V. R. N. S. P. (2026). . Pathophysiology of Cell Injury Journal (PCIJ), 15(1), 1-18. https://pcij.net/archives/2248
Rajesh Kumar Sharma, Anjali Mehta, Vivek Reddy Narayan, Sneha Patel. \".\" Pathophysiology of Cell Injury Journal (PCIJ), vol. 15, no. 1, 2026, pp. 1-18. https://pcij.net/archives/2248
Rajesh Kumar Sharma, Anjali Mehta, Vivek Reddy Narayan, Sneha Patel. . Pathophysiology of Cell Injury Journal (PCIJ). 2026;15(1):1-18. https://pcij.net/archives/2248
Rajesh Kumar Sharma, Anjali Mehta, Vivek Reddy Narayan, Sneha Patel (2026) . Pathophysiology of Cell Injury Journal (PCIJ), 15(1), pp. 1-18. Available at: https://pcij.net/archives/2248
@article{rajesh-kumar-sharma-anjali-mehta-vivek-reddy-narayan-sneha-patel-2026, title = {}, author = {Rajesh Kumar Sharma, Anjali Mehta, Vivek Reddy Narayan, Sneha Patel}, journal = {Pathophysiology of Cell Injury Journal (PCIJ)}, year = {2026}, volume = {15}, number = {1}, pages = {1-18}, url = {https://pcij.net/archives/2248}, }
TY - JOUR AU - Rajesh Kumar Sharma, Anjali Mehta, Vivek Reddy Narayan, Sneha Patel TI - JO - Pathophysiology of Cell Injury Journal (PCIJ) PY - 2026 VL - 15 IS - 1 SP - 1 EP - 18 UR - https://pcij.net/archives/2248 ER -

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