Atherosclerosis is a complex inflammatory process associated with high-mortality cardiovascular diseases. Today, there is a growing body of evidence linking atherosclerosis to mutations of mitochondrial DNA (mtDNA). But the mechanism of this link is insufficiently studied. Atherosclerosis progression involves different cell types and macrophages are one of the most important. Due to their high plasticity, macrophages can demonstrate pro-inflammatory and pro-atherogenic (macrophage type M1) or anti-inflammatory and anti-atherogenic (macrophage type M2) effects. These two cell types, formed as a result of external stimuli, differ significantly in their metabolic profile, which suggests the central role of mitochondria in the implementation of the macrophage polarization route. According to this, we assume that mtDNA mutations causing mitochondrial disturbances can play the role of an internal trigger, leading to the formation of macrophage M1 or M2. This review provides a comparative analysis of the characteristics of mitochondrial function in different types of macrophages and their possible associations with mtDNA mutations linked with inflammation-based pathologies including atherosclerosis.
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http://dx.doi.org/10.3390/ijms26031019 | DOI Listing |
Int Immunopharmacol
March 2025
School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China. Electronic address:
Atherosclerosis is a chronic inflammatory disease in which mitochondrial DNA (mtDNA) has emerged as a key contributor to its pathogenesis. We synthesized evidence from experimental and clinical studies showing that mtDNA damage, release, and mutation profoundly affect endothelial cells, macrophages, and vascular smooth muscle cells, thereby driving plaque initiation and progression. By activating immune signaling pathways-including cGAS-STING, NLRP3 inflammasome, and TLR9-mtDNA amplifies inflammation and oxidative stress, exacerbating atherosclerotic lesion development.
View Article and Find Full Text PDFSci Adv
March 2025
Department of Radiation Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Lung cancer exhibits altered metabolism, influencing its response to radiation. To investigate the metabolic regulation of radiation response, we conducted a comprehensive, metabolic-wide CRISPR-Cas9 loss-of-function screen using radiation as selection pressure in human non-small cell lung cancer. Lipoylation emerged as a key metabolic target for radiosensitization, with lipoyltransferase 1 (LIPT1) identified as a top hit.
View Article and Find Full Text PDFHeliyon
February 2025
Genetics and Molecular Biology branch, Department of Zoology, University of Dhaka, Dhaka, 1000, Bangladesh.
Budding yeast, is an ideal model organism for genetic research due to its similarity in life cycle and cellular structure to higher eukaryotes as well as its ease of cultivation and manipulation in the laboratory. Yeast cells benefit from being cultured in calorie-restricted media, which can be achieved by reducing glucose concentration from 2 % to 0.5 %.
View Article and Find Full Text PDFNat Neurosci
March 2025
State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Amyotrophic lateral sclerosis (ALS) is categorized into ~10% familial and ~90% sporadic cases. While familial ALS is caused by mutations in many genes of diverse functions, the underlying pathogenic mechanisms of ALS, especially in sporadic ALS (sALS), are largely unknown. Notably, about half of the cases with sALS showed defects in mitochondrial respiratory complex IV (CIV).
View Article and Find Full Text PDFYi Chuan
March 2025
Senior Department of Otolaryngology-Head & Neck Surgery, the Sixth Medical Center of PLA General Hospital, Beijing 100048,China.
mutations (DNMs) are significant genetic factors contributing to sporadic hearing loss (HL) and complex HL syndromes. To analyze the genetic counseling characteristics and interpretation of pathogenic DNMs for sporadic HL, we retrospectively analyze the clinical information of probands and their parents from 410 sporadic HL core pedigrees enrolled in the "Chinese Deafness Genome Project (CDGP)" between October 2015 and October 2023. We apply family trio-based genome sequencing (targeted gene capture and high throughput sequencing, mitochondrial genome sequencing, and copy number variants analysis) and validate the samples of their unaffected-parents.
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