ReviewFunctional & integrative genomics2026
Mitochondrial dysfunction in hypertension: mechanistic pathways and therapeutic implications.
Review in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Hypertension is a major global cardiovascular disorder characterized by complex and multifactorial pathogenesis. Although numerous antihypertensive therapies are available, a considerable proportion of patients continue to exhibit inadequate blood pressure control. Emerging evidence underscores the central role of mitochondrial dysfunction in the development and progression of hypertension. As regulators of energy metabolism, redox balance, calcium signaling, and cell survival, mitochondria play a significant role in maintaining vascular and neuronal homeostasis. Mitochondrial abnormalities-such as excessive ROS production, impaired mitophagy, disrupted fusion and fission dynamics, and calcium dysregulation—can amplify vascular dysfunction and sympathetic overactivation, thereby elevating blood pressure. This review summarizes current advances in mitochondrial pathophysiology in hypertension and discusses mitochondrial-targeted therapeutic strategies. Natural products derived from traditional Chinese medicine (e.g., apigenin, berberine, curcumin) and Western compounds (e.g., MitoTEMPO, empagliflozin, Mdivi-1) show promise in mitigating mitochondrial stress and lowering blood pressure. A deeper understanding of mitochondria-centered mechanisms may offer novel opportunities for precision therapy, particularly in resistant hypertension.
Indexed as
Identifiers
41656396What Socratic 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 Socratic graph.