Ask about this productRelated genes to: CHCHD6 Blocking Peptide
- Gene:
- CHCHD6 NIH gene
- Name:
- coiled-coil-helix-coiled-coil-helix domain containing 6
- Previous symbol:
- -
- Synonyms:
- MGC13016, PPP1R23, CHCM1, Mic25, MICOS25
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-19
- Date modifiied:
- 2018-11-16
Related products to: CHCHD6 Blocking Peptide
Related articles to: CHCHD6 Blocking Peptide
- Cartilage calcification actively contributes to osteoarthritis progression by generating mineral depositions that disrupt joint homeostasis and amplify matrix degradation. Previous studies found that chondrocyte-derived matrix vesicles provide the minerals orchestrating pathological cartilage calcification. However, the intracellular origin of minerals in osteoarthritic cartilage remains elusive, significantly impeding the development of targeted therapies. This study identified mitochondria as subcellular reservoirs of mineral precursors containing calcium and phosphorus. At the early stage of osteoarthritis, chondrocyte mitochondrial DNA (mtDNA) is transformed into an intertwined state that enables them to stabilize minerals into amorphous precursors. The stabilized amorphous mineral precursors are then transported via vesicles to the mineralization site. Targeting mtDNA distribution by modulating coiled-coil-helix, coiled-coil-helix-domain containing 6 (CHCHD6) can inhibit cartilage calcification and impair osteoarthritis progression. Our findings provide mechanistic insights into mitochondrial orchestration of incipient pathological cartilage calcification in osteoarthritis. Elucidating the mitochondrial-driven calcification cascade redefines therapeutic paradigms, enabling rational design of mineralization-inhibitory strategies for early management of osteoarthritis. - Source: PubMed
Publication date: 2026/02/28
Wan QianqianYe TaoGu JuntingMa YuxuanQin WenYan JianfeiRao JinChen LeiHao DongxiaoTay Franklin RJiao KaiNiu Lina - We aimed to identify the key proteins of miR-142-3p that regulate ferroptosis and ultimately control the downstream effectors of cardiomyocyte growth. - Source: PubMed
Publication date: 2025/09/20
Gao NingWu Peng-FeiWu Ming-WenLi Yu-MengLiang XuWang Fei-FeiLi Xue-JingShen Qing-QingZheng Tian-PengLiu Xiao-LingSun YiYang Liu-Xue - The present study aimed to clarify the clinical significance of the cell-free DNA (cfDNA) methylation profile of patients with non-small cell lung cancer (NSCLC) showing the epidermal growth factor receptor (EGFR) gene mutation. - Source: PubMed
Publication date: 2025/04/25
Fujimoto MaoYasuda HiroyukiArai EriNakajima MakotoTakata SaoriMorikawa KeiTanaka HisashiItani HidetoshiHonda TakeshiHoriuchi KazuyaWatanabe KageakiNakagawa HideyukiNakahara YoshiroSeki YoshitakaBessho AkihiroTakahashi NobumasaHayashi KentaroEndo TakeoTakeyama KiyoshiMaekura ToshiyaTakigawa NagioKawase AkikazuEndoh MakotoNemoto KenjiKishi KazumaSoejima KenzoOkuma YusukeTogashi AkiraMatsutani NoriyukiSeki NobuhikoKanai Yae - During aging, muscle gradually undergoes sarcopenia, the loss of function associated with loss of mass, strength, endurance, and oxidative capacity. However, the 3D structural alterations of mitochondria associated with aging in skeletal muscle and cardiac tissues are not well described. Although mitochondrial aging is associated with decreased mitochondrial capacity, the genes responsible for the morphological changes in mitochondria during aging are poorly characterized. We measured changes in mitochondrial morphology in aged murine gastrocnemius, soleus, and cardiac tissues using serial block-face scanning electron microscopy and 3D reconstructions. We also used reverse transcriptase-quantitative PCR, transmission electron microscopy quantification, Seahorse analysis, and metabolomics and lipidomics to measure changes in mitochondrial morphology and function after loss of mitochondria contact site and cristae organizing system (MICOS) complex genes, Chchd3, Chchd6, and Mitofilin. We identified significant changes in mitochondrial size in aged murine gastrocnemius, soleus, and cardiac tissues. We found that both age-related loss of the MICOS complex and knockouts of MICOS genes in mice altered mitochondrial morphology. Given the critical role of mitochondria in maintaining cellular metabolism, we characterized the metabolomes and lipidomes of young and aged mouse tissues, which showed profound alterations consistent with changes in membrane integrity, supporting our observations of age-related changes in muscle tissues. We found a relationship between changes in the MICOS complex and aging. Thus, it is important to understand the mechanisms that underlie the tissue-dependent 3D mitochondrial phenotypic changes that occur in aging and the evolutionary conservation of these mechanisms between Drosophila and mammals. - Source: PubMed
Publication date: 2023/11/13
Vue ZerGarza-Lopez EdgarNeikirk KitKatti PrasannaVang LarryBeasley HeatherShao JianqiangMarshall Andrea GCrabtree AmberMurphy Alexandria CJenkins Brenita CPrasad PraveenaEvans ChantellTaylor BrittanyMungai MargaretKillion MasonStephens DominiqueChristensen Trace ALam JacobRodriguez BenjaminPhillips Mark ADaneshgar NastaranKoh Ho-JinKoh AliceDavis JamaineDevine NinaSaleem MohammadScudese EstevãoArnold Kenneth RyanVanessa Chavarin ValeriaDaniel Robinson RyanChakraborty MoumitaGaddy Jennifer ASweetwyne Mariya TWilson GenesisZaganjor ElmaKezos JamesDondi CristianaReddy Anilkumar KGlancy BrianKirabo AnnetQuintana Anita MDai Dao-FuOcorr KarenMurray Sandra ADamo Steven MExil VernatRiggs BlakeMobley Bret CGomez Jose AMcReynolds Melanie RHinton Antentor - With sparse treatment options, cardiac disease remains a significant cause of death among humans. As a person ages, mitochondria breakdown and the heart becomes less efficient. Heart failure is linked to many mitochondria-associated processes, including endoplasmic reticulum stress, mitochondrial bioenergetics, insulin signaling, autophagy, and oxidative stress. The roles of key mitochondrial complexes that dictate the ultrastructure, such as the mitochondrial contact site and cristae organizing system (MICOS), in aging cardiac muscle are poorly understood. To better understand the cause of age-related alteration in mitochondrial structure in cardiac muscle, we used transmission electron microscopy (TEM) and serial block facing-scanning electron microscopy (SBF-SEM) to quantitatively analyze the three-dimensional (3-D) networks in cardiac muscle samples of male mice at aging intervals of 3 mo, 1 yr, and 2 yr. Here, we present the loss of cristae morphology, the inner folds of the mitochondria, across age. In conjunction with this, the three-dimensional (3-D) volume of mitochondria decreased. These findings mimicked observed phenotypes in murine cardiac fibroblasts with CRISPR/Cas9 knockout of (some members of the MICOS complex), and , which showed poorer oxidative consumption rate and mitochondria with decreased mitochondrial length and volume. In combination, these data show the need to explore if loss of the MICOS complex in the heart may be involved in age-associated mitochondrial and cristae structural changes. This article shows how mitochondria in murine cardiac changes, importantly elucidating age-related changes. It also is the first to show that the MICOS complex may play a role in outer membrane mitochondrial structure. - Source: PubMed
Publication date: 2023/08/25
Vue ZerNeikirk KitVang LarryGarza-Lopez EdgarChristensen Trace AShao JianqiangLam JacobBeasley Heather KMarshall Andrea GCrabtree AmberAnudokem JosephsRodriguez BenjaminKirk BenjaminBacevac SerifBarongan TaylorShao BryannaStephens Dominique CKabugi KinuthiaKoh Ho-JinKoh AliceEvans Chantell STaylor BrittanyReddy Anilkumar KMiller-Fleming TyneActkins Ky'Era VZaganjor ElmaDaneshgar NastaranMurray Sandra AMobley Bret CDamo Steven MGaddy Jennifer ARiggs BlakeWanjalla CelestineKirabo AnnetMcReynolds MelanieGomez Jose APhillips Mark AExil VernatDai Dao-FuHinton Antentor