<?xml version="1.0" encoding="UTF-8"?>
<doi_batch xmlns="http://www.crossref.org/schema/4.4.2" version="4.4.2" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:jats="http://www.ncbi.nlm.nih.gov/JATS1" xsi:schemaLocation="http://www.crossref.org/schema/4.4.2 http://www.crossref.org/schemas/crossref4.4.2.xsd">
  <head>
    <doi_batch_id>pcij-2248-1775655832</doi_batch_id>
    <timestamp>20260408134352</timestamp>
    <depositor>
      <depositor_name>PCIJ</depositor_name>
      <email_address>bmpublisher@bmpublisher.net</email_address>
    </depositor>
    <registrant>Pathophysiology of Cell Injury Journal</registrant>
  </head>
  <body>
    <journal>
      <journal_metadata>
        <full_title>Pathophysiology of Cell Injury Journal</full_title>
        <issn media_type="electronic">2378-5225</issn>
      </journal_metadata>
      <journal_issue>
        <journal_volume>
          <volume>15</volume>
        </journal_volume>
        <issue>1</issue>
        <publication_date media_type="online">
          <year>2026</year>
          <month>1</month>
          <day>3</day>
        </publication_date>
      </journal_issue>
      <journal_article publication_type="full_text">
        <titles>
          <title>Myeloid Cell–Driven Inflammatory Responses Exacerbate Myocardial Cell Injury in Mice</title>
        </titles>
        <contributors>
          <person_name contributor_role="author" sequence="first">
            <given_name>Rajesh Kumar</given_name>
            <surname>Sharma</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <given_name>Anjali</given_name>
            <surname>Mehta</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <given_name>Vivek Reddy</given_name>
            <surname>Narayan</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <given_name>Sneha</given_name>
            <surname>Patel</surname>
          </person_name>
        </contributors>
        <jats:abstract xmlns:jats="http://www.ncbi.nlm.nih.gov/JATS1">
          <jats:p>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.</jats:p>
        </jats:abstract>
        <publication_date media_type="online">
          <year>2026</year>
          <month>1</month>
          <day>3</day>
        </publication_date>
        <doi_data>
          <doi>10.18081/2378-5225/15.1</doi>
          <resource>https://pcij.net/archives/2248</resource>
        </doi_data>
      </journal_article>
    </journal>
  </body>
</doi_batch>
