Most TUDCA research on the heart and circulation looks at blood pressure, endothelial function or heart muscle. A separate set of animal studies asks a more structural question: can TUDCA change what happens inside an artery wall after injury, under a high-cholesterol diet or when the wall weakens? In rats with a balloon-injured carotid artery, oral TUDCA reduced the thickening of the inner wall [1]. In rabbits fitted with carotid stents, TUDCA lowered in-stent narrowing [2]. In cholesterol-prone mice, it reduced plaque area [3] and the diameter of angiotensin-induced abdominal aortic aneurysms [4]. These are consistent results, but all of them come from animals, and no study has measured artery narrowing, plaque or aneurysm growth in people taking TUDCA. This page walks through each study and what it can and cannot support.
Key Takeaways
- In rats with balloon-injured carotid arteries, oral TUDCA reduced the intima-to-media ratio by slowing smooth muscle cell growth and inducing their apoptosis [1].
- In 18 rabbits on an atherogenic diet, carotid stents combined with TUDCA had the lowest percent stenosis at 28 days: 28% versus 35% for a drug-eluting Firebird stent and 40% for a bare metal stent [2].
- A TUDCA-releasing nanoparticle stent coating sped up the regrowth of the artery lining in rabbits [5].
- In ApoE-deficient mice, TUDCA reduced arterial plaque area and improved cholesterol efflux from macrophages [3], and it reduced the maximum diameter of angiotensin II-induced abdominal aortic aneurysms [4].
- No human trial has tested TUDCA for restenosis, atherosclerosis or aneurysm. TUDCA effects on human endothelial function are a separate question covered on our blood pressure page.
Why Artery Walls Are Part of the ER Stress Story
An artery wall has three layers. The inner lining, the endothelium, is a single sheet of cells that controls clotting and vessel tone. The middle layer is made of smooth muscle cells, and the outer layer is connective tissue. Many artery problems come down to these cells behaving badly: smooth muscle cells multiplying and migrating inward after an injury, macrophages filling with cholesterol to form plaque, or smooth muscle cells dying and the wall weakening into an aneurysm.
Each of these processes has been linked to endoplasmic reticulum stress, the strain that builds up when cells cannot fold proteins as fast as they need them. TUDCA is a chemical chaperone that eases ER stress in laboratory models, so researchers have used it to ask whether calming that stress changes how an artery responds. That is why it shows up in this literature, not because it was developed as a heart drug.
Restenosis: Narrowing After Balloon Injury and Stents
When a narrowed artery is opened with a balloon or a stent, the vessel can narrow again over the following months. The main driver is neointimal hyperplasia, a buildup of smooth muscle cells that grow and migrate into the inner layer. This is called restenosis, and modern drug-eluting stents release drugs that slow that growth.
Balloon injury in rats. A 2011 study first showed that human vascular smooth muscle cells take up TUDCA through a transporter called OATP2, and that TUDCA reduced their viability and migration in culture by suppressing ERK signaling [1]. Rats with a balloon-injured carotid artery then received oral TUDCA. It reduced the injury-induced rise in ERK and the enzyme MMP-9 and significantly decreased the ratio of the thickened inner layer to the middle layer, by reducing smooth muscle cell proliferation and inducing their apoptosis [1]. This is one of the few vascular studies where the abstract states oral dosing, although it does not give the dose.
Stents in rabbits. A 2019 study fed 18 rabbits an atherogenic diet and implanted bare metal stents, bare metal stents plus TUDCA, or Firebird drug-eluting stents in the carotid artery [2]. After 28 days, neointimal area was lowest with bare metal stents plus TUDCA (1.6 mm²), compared with 1.90 mm² for Firebird and 2.3 mm² for bare metal. Percent stenosis followed the same order: 28%, 35% and 40% [2]. In culture, TUDCA reduced smooth muscle cell growth and migration and lowered ER stress markers across a range of 10 to 1000 μmol/L. The paper’s title describes TUDCA as an oral drug, but the abstract does not state the dose or how it was given, and with 18 rabbits split three ways, each group was small.
A TUDCA stent coating. A 2022 study took a different route and built stents coated with biodegradable nanoparticles that released TUDCA slowly over 28 days [5]. In rabbits, these stents sped up re-endothelialization, the regrowth of the protective inner lining over the stent, and in cultured endothelial cells TUDCA reduced apoptosis caused by oxidative stress [5]. This is a device result. The TUDCA was delivered directly into the artery wall from the stent, which is not something a capsule can do.
Atherosclerotic Plaque
Atherosclerosis begins when cholesterol-carrying particles lodge in the artery wall and macrophages swallow them, turning into lipid-filled foam cells that build plaque. A 2024 study used ApoE-deficient mice, a standard model that develops plaque on a high-fat diet, and treated some of them with TUDCA [3]. TUDCA reduced plaque area in the artery, lowered inflammasome activation and improved cholesterol efflux, the ability of macrophages to export cholesterol. In cell experiments, it blocked oxidized LDL from turning macrophages into foam cells by acting on the PERK/eIF2α/ATF4 pathway and the AIM2 inflammasome [3].
A related 2023 study looked at arteriovenous grafts, the surgical connections used for dialysis access, in mice on a high-fat diet [6]. Here TUDCA was used only in cultured endothelial cells, where it reversed the barrier damage caused by oxidized LDL. The reduction in graft narrowing in living mice came from deleting the CHOP gene, not from TUDCA [6]. It supports the idea that ER stress in the artery lining matters, but it is not evidence that TUDCA protected a graft in an animal.
Abdominal Aortic Aneurysm
An abdominal aortic aneurysm is a ballooning of the main artery in the abdomen. It grows as smooth muscle cells die, inflammatory cells invade and the elastic fibers of the wall break down, and a large aneurysm can rupture. A 2017 study first examined human aneurysm tissue and found that the ER stress chaperones GRP78 and GRP94 were significantly higher in aneurysmal areas than in normal aorta [4].
The researchers then used ApoE-deficient mice given angiotensin II, which reliably produces abdominal aneurysms. TUDCA significantly reduced the maximum diameter of the abdominal aorta, lowered ER stress chaperones, reduced the number of dying cells and decreased a range of apoptosis signals including caspase-3, caspase-12 and CHOP [4]. The human part of this study measured tissue taken from aneurysms. No one with an aneurysm was given TUDCA, and the abstract does not report whether TUDCA affected rupture.
What This Means for Your Arteries
Across these studies, the pattern is the same: in rats, rabbits and mice, TUDCA calmed ER stress in artery wall cells and reduced narrowing after injury, plaque area or aneurysm size. That is a reasonable basis for further research. It is not a basis for using TUDCA to protect a stent, slow atherosclerosis or manage an aneurysm. The animal models compress years of human disease into weeks, the doses were chosen for rodents and rabbits, and the stent coating study delivered TUDCA directly into the vessel wall.
People who have a stent, known coronary disease or an aneurysm are usually on medications with strong human evidence, such as antiplatelet drugs and statins, along with blood pressure control and scheduled imaging. TUDCA has not been tested alongside those treatments, and its effects on bleeding risk or drug interactions in this setting have not been studied. If you are considering it, treat it as an unproven addition, discuss it with your cardiologist or vascular surgeon, and never stop or reduce prescribed cardiovascular medication because of it.
Bottom Line
Oral TUDCA reduced inner-wall thickening after balloon injury in rats [1], TUDCA lowered in-stent narrowing in a small rabbit study [2], and a TUDCA-releasing stent coating sped up healing of the artery lining [5]. In ApoE-deficient mice it reduced plaque area [3] and aneurysm diameter [4], while the graft narrowing result in mice belonged to a CHOP gene deletion rather than TUDCA [6]. No human study has measured restenosis, plaque or aneurysm growth with TUDCA, so these remain animal findings.
Frequently Asked Questions
Does TUDCA prevent restenosis after a stent?
Only animal data exist. Oral TUDCA reduced inner-wall thickening after balloon injury in rats [1], and in 18 rabbits stents plus TUDCA had 28% stenosis versus 40% with bare metal stents [2]. No human trial has tested it, and it is not a replacement for the medication prescribed after a stent.
Can TUDCA reduce arterial plaque?
In ApoE-deficient mice on a high-fat diet, TUDCA reduced plaque area and improved cholesterol efflux from macrophages [3]. That is a mouse result. No study has measured plaque in people taking TUDCA.
Does TUDCA help with an abdominal aortic aneurysm?
It reduced aneurysm diameter in angiotensin II-treated ApoE-deficient mice, and ER stress chaperones were raised in human aneurysm tissue [4]. No one with an aneurysm has been treated with TUDCA in a study, and aneurysm care depends on monitoring and, when needed, surgical repair.
References
- Kim SY, et al. Tauroursodeoxycholate (TUDCA) inhibits neointimal hyperplasia by suppression of ERK via PKCα-mediated MKP-1 induction. Cardiovascular Research (2011). PMID 21840882
- Luo H, et al. The Role of Tauroursodeoxycholic Acid on Dedifferentiation of Vascular Smooth Muscle Cells by Modulation of Endoplasmic Reticulum Stress and as an Oral Drug Inhibiting In-Stent Restenosis. Cardiovascular Drugs and Therapy (2019). PMID 30663009
- Wang X, et al. TUDCA alleviates atherosclerosis by inhibiting AIM2 inflammasome and enhancing cholesterol efflux capacity in macrophage. iScience (2024). PMID 38784008
- Qin Y, et al. Tauroursodeoxycholic Acid Attenuates Angiotensin II Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-deficient Mice by Inhibiting Endoplasmic Reticulum Stress. European Journal of Vascular and Endovascular Surgery (2017). PMID 27889204
- Zhou J, et al. Repair effect of the poly (D,L-lactic acid) nanoparticle containing tauroursodeoxycholic acid-eluting stents on endothelial injury after stent implantation. Frontiers in Cardiovascular Medicine (2022). PMID 36426231
- Zhong YX, et al. Endoplasmic Reticulum Stress-induced Endothelial Dysfunction Promotes Neointima Formation after Arteriovenous Grafts in Mice on High-fat Diet. Current Medical Science (2023). PMID 36640244
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These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.
