ArticleProceedings of the National Academy of Sciences of the United States of America2013
Higd-1a interacts with Opa1 and is required for the morphological and functional integrity of mitochondria.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- Far-infrared irradiation restores mitochondrial dynamics to ameliorate ischemic stroke.Neural regeneration research · 2026Article
- Amyloid-Forming Amylin Secreted by the Pancreas Promotes Hypoxia-Inducible Factor Activation and Mitochondrial Alterations in Liver and Heart During Type 2 Diabetes Pathogenesis.Comprehensive physiology · 2026Article
- HIGD1A Alleviates Oxidative Stress Related Ovarian Hypofunction by Enhancing Granulosa Cell Functions via NF-κB/SOD2 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Differential Gene Expression Analysis in a Lumbar Spinal Stenosis Rat Model via RNA Sequencing: Identification of Key Molecular Pathways and Therapeutic Insights.Biomedicines · 2025Article
- The functional role of Higd1a in mitochondrial homeostasis and in multiple disease processes.Genes & diseases · 2023Review
- Hypoxia-reprogramed megamitochondrion contacts and engulfs lysosome to mediate mitochondrial self-digestion.Nature communications · 2023Article
- Developmental programming: adverse sexually dimorphic transcriptional programming of gestational testosterone excess in cardiac left ventricle of fetal sheep.Scientific reports · 2023Article
- Enhanced hepatic respiratory capacity and altered lipid metabolism support metabolic homeostasis during short-term hypoxic stress.BMC biology · 2021Article
- HIG1 domain family member 1A disrupts proliferation, migration, and invasion of colon adenocarcinoma cells.Bioengineered · 2021Article
- Computational Approaches for Cancer-Fighting: From Gene Expression to Functional Foods.Cancers · 2021Article
- HIGD‑1B inhibits hypoxia‑induced mitochondrial fragmentation by regulating OPA1 cleavage in cardiomyocytes.Molecular medicine reports · 2021Article
- Review
- OMA1 reprograms metabolism under hypoxia to promote colorectal cancer development.EMBO reports · 2021Article
- HIGD-Driven Regulation of CytochromeCells · 2020Review
- Three-dimensional electron microscopy techniques for unravelling mitochondrial dysfunction in heart failure and identification of new pharmacological targets.British journal of pharmacology · 2019Review
- Integrating Gene and Protein Expression Reveals Perturbed Functional Networks in Alzheimer's Disease.Cell reports · 2019Article
- Higd1a Protects Cells from Lipotoxicity under High-Fat Exposure.Oxidative medicine and cellular longevity · 2019Article
- The Expression of Hypoxia-Induced Gene 1 (Higd1a) in the Central Nervous System of Male and Female Rats Differs According to Age.Journal of molecular neuroscience : MN · 2018Article
- miR-375 down-regulation of the rearranged L-myc fusion and hypoxia-induced gene domain protein 1A genes and effects on Sertoli cell proliferation.Asian-Australasian journal of animal sciences · 2018Article
- TLR4 Activation Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy by Inducing Mitochondrial Dynamic Imbalance.Oxidative medicine and cellular longevity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity and morphology of mitochondria are maintained by dynamic fusion and fission processes regulated by a group of proteins residing in, or attached to, their inner and outer membranes. Hypoxia-induced gene domain protein-1a (Higd-1a)/HIMP1-a/HIG1, a mitochondrial inner membrane protein, plays a role in cell survival under hypoxic conditions. In the present study, we showed that Higd-1a depletion resulted in mitochondrial fission, depletion of mtDNA, disorganization of cristae, and growth retardation. We demonstrated that Higd-1a functions by specifically binding to Optic atrophy 1 (Opa1), a key element in fusion of the inner membrane. In the absence of Higd-1a, Opa1 was cleaved, resulting in the loss of its long isoforms and accumulation of small soluble forms. The small forms of Opa1 do not interact with Higd-1a, suggesting that a part of Opa1 in or proximal to the membrane is required for that interaction. Opa1 cleavage, mitochondrial fission, and cell death induced by dissipation of the mitochondrial membrane potential were significantly inhibited by ectopic expression of Higd-1a. Furthermore, growth inhibition due to Higd-1a depletion could be overcome by overexpression of a noncleavable form of Opa1. Collectively, our observations demonstrate that Higd-1a inhibits Opa1 cleavage and is required for mitochondrial fusion by virtue of its interaction with Opa1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.