Evidence mapPaperPMID 42368857Full record

ReviewFrontiers in cardiovascular medicine2026

Molecular Interplay between hypertension and dyslipidemia in cardiovascular pathogenesis: toward precision-based therapeutic strategies.

Boming Cao, Jingyi Pei, Ling Kong, Ying Han, Guangli Yan, Xijun Wang

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Boming CaoState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.
Jingyi PeiState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.
Ling KongState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.
Ying HanState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.
Guangli YanState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.
Xijun WangState Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) remains the foremost cause of global mortality. Hypertension and dyslipidemia, frequently coexisting, exert synergistic effects that substantially elevate CVD risk via interconnected molecular pathways. This review systematically examines the synergistic mechanisms underlying their combined contribution to CVD progression, with a focus on key pathways such as the RAAS/PPAR axis, AMPK/SIRT1 signaling, and NLRP3 inflammasome activation. We highlight how their interplay disrupts endothelial function, aggravates oxidative stress, and promotes chronic inflammation, thereby causing vascular damage and atherosclerosis. Furthermore, we examine emerging targeted therapies, including the combination of RAAS inhibitors with statins, PCSK9 inhibitors, as well as newer agents such as SGLT2 inhibitors and GLP-1 receptor agonists. These approaches represent promising multi-target strategies for improving clinical outcomes. Ultimately, this review underscores the need for a precision medicine framework that addresses the synergistic pathophysiology of hypertension and dyslipidemia, paving the way for personalized, pathway-integrated interventions aimed at restoring metabolic-vascular homeostasis rather than merely treating disease.

Indexed as

cardiovascular diseasedyslipidemiahypertensioninflammationmolecular mechanismstargeted therapy

Identifiers

PMID42368857
PMCPMC13294277

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.