Revealing Cell-Free Mitochondrial DNA Breakage Patterns as Novel Biomarkers for Sepsis.

Accurate early diagnosis and prognosis of sepsis remain major clinical challenges. This study explores specific plasma cell-free mitochondrial DNA (cfmtDNA) breakage patterns as potential biomarkers for sepsis. Plasma samples from ten non-sepsis control patients and 63 sepsis patients are analyzed using mitochondrial DNA fragmentomics, revealing distinct breakage sites in the RNR2 (positions 2474-2478) and COX2 (positions 7761, 7775, 7776, 7777, and 7783) regions, which are intact in healthy individuals but exhibited high-frequency breakage in sepsis patients.

TSPO exacerbates sepsis-induced cardiac dysfunction by inhibiting p62-Mediated autophagic flux via the ROS-RIP1/RIP3-exosome axis.

Septic cardiomyopathy (SCM) is a critical complication of sepsis, primarily attributed to mitochondrial dysfunction and impaired autophagic flux. This study explores the role of translocator protein (TSPO) in SCM pathogenesis and assesses its potential as a therapeutic target. We identified increased TSPO expression in plasma samples from sepsis patients, with further validation in septic rats and LPS-stimulated H9C2 cardiomyocytes.

Global longitudinal strain and the risk of major adverse cardiac events in post-myocardial infarction patients: A retrospective cohort study.

Background: This study evaluates the relationship between global longitudinal strain (GLS) and late major adverse cardiovascular events (MACEs) in patients after acute myocardial infarction (AMI).

Methods: Data of newly diagnosed AMI patients between March 2010 and July 2014 were retrospectively evaluated. The patients underwent serial echocardiography at admission and at third and sixth months post-admission.

PGC-1α loss promotes mitochondrial protein lactylation in acetaminophen-induced liver injury via the LDHB-lactate axis.

Coronavirus disease 2019 (COVID-19) affected people worldwide, and fever is one of the major symptoms of this disease. Although Acetaminophen (APAP) is a common fever-reducing medication, it can also mediate liver injury. However, the role of PGC-1α in regulating mitochondrial quality control by lactate dehydrogenase B (LDHB), a vital enzyme catalyzing the conversion of lactate to pyruvate, in APAP-induced hepatotoxicity, is unclear.