The current outlook is: Dietary cholesterol is largely a non-issue still overburdened with much anxiety and even hysteria. While certain levels and ratios of "blood cholesterol" (different lipoproteins, triglycerides etc.) are still treated as indicators of possible trouble that may call for intervention, that intervention is likely pharmacological in nature and less through dietary means of reducing cholesterol intake. Dietary cholesterol is not "The Bad Guy" to avoid at all costs.
So, no, eating (too much) cholesterol is not that bad in itself. (But keep in mind that 'eating too much cholesterol' may be the result of eating too much and too fat in general. That is bad.) The type of natural fat ingested is less important over-all and even blood cholesterol or lipo-proteins are under fire as being much less of a value in predicting health outcomes or even being a worthy target to intervene at all:
People with high cholesterol live the longest.
And that might almost explain why decreasing cholesterol intake leads to an increase in the absorption rate and an increase in cholesterol synthesis.
Jean-Michel Lecerf and Michel de Lorgeril: "Dietary cholesterol: from physiology to cardiovascular risk", British Journal of Nutrition, Volume 106, Issue 1, 14 July 2011, pp. 6-14, https://doi.org/10.1017/S0007114511000237:
Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low. Given the necessity for cholesterol, very effective intestinal uptake mechanisms and enterohepatic bile acid and cholesterol reabsorption cycles exist; conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper-absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD. Recent biological data concerning the effect of dietary cholesterol on LDL receptor-related protein may explain the complexity of the effect of cholesterol on CVD risk. [emphasis added]
Mitchell M. Kanter, et al.: "Exploring the Factors That Affect Blood Cholesterol and Heart Disease Risk: Is Dietary Cholesterol as Bad for You as History Leads Us to Believe?", Advances in Nutrition, September 2012, vol. 3: 711-717, doi: 10.3945/an.111.001321:
For much of the past 50 years, a great deal of the scientific literature regarding dietary fat and cholesterol intake has indicated a strong positive correlation with heart disease. In recent years, however, there have been a number of epidemiological studies that did not support a relationship between cholesterol intake and cardiovascular disease. Further, a number of recent clinical trials that looked at the effects of long-term egg consumption (as a vehicle for dietary cholesterol) reported no negative impact on various indices of cardiovascular health and disease. Coupled with data indicating that the impact of lowering dietary cholesterol intake on serum LDL levels is small compared with other dietary and lifestyle factors, there is a need to consider how otherwise healthy foods can be incorporated in the diet to meet current dietary cholesterol recommendations. Because eggs are a healthful food, it is particularly important that sensible strategies be recommended for inclusions of eggs in a healthy diet.
Samantha Berger et al.: "Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis", American Journal of Clinical Nutrition, 102: 235-236; July 15, 2015, doi: 10.3945/ajcn.114.100305:
Forty studies (17 cohorts in 19 publications with 361,923 subjects and 19 trials in 21 publications with 632 subjects) published between 1979 and 2013 were eligible for review. […] Dietary cholesterol was not statistically significantly associated with any coronary artery disease […] or hemorrhagic stroke. […] Dietary cholesterol did not statistically significantly change serum triglycerides or very-low-density lipoprotein concentrations. Reviewed studies were heterogeneous and lacked the methodologic rigor to draw any conclusions regarding the effects of dietary cholesterol on CVD risk. Carefully adjusted and well-conducted cohort studies would be useful to identify the relative effects of dietary cholesterol on CVD risk.
Erik Rifkin, Edward Bouwery: "The Illusion of Certainty [Health Benefits and Risks]", Springer, New York, 2007,
chap 8: "Elevated Cholesterol: A Primary Risk Factor for Heart Disease?", p. 91:
But let’s assume for a moment that Fig. 8.1 is correct. Let’s say the gentle upward trend from the lowest to the highest cholesterol level is legitimate. Let’s forget about difficulties in excluding diabetics and people with genetic abnormalities, and in normalizing for age and unknown additive or synergistic effects of multiple risk factors. Then in a group of 1,000 individuals with elevated cholesterol, there will be approximately 1 additional death annually when compared to 1,000 individuals with normal cholesterol. Therefore, 99.9% of the individuals with elevated cholesterol would not be affected. [emphasis added]
That is important: just assuming the hypothesis once taken for granted: "eating eggs clogs your arteries" (the so called "diet-heart hypothesis") is correct does not translate well into statistical observations for the general population or public health.
To give an outdated but relatable picture to this statistical figure:
"1987 wies S. Seely nach, daß eine lebenslang durchgehaltene cholesterinarme Kost die Lebensdauer lediglich um drei Tage bis drei Monate, bestenfalls jedoch um ein Jahr erhöhe." (Translation: Seely had proven in 1987 that lifelong avoidance of dietary cholesterol would lead to prolongation of a life by just 3 days to 3 months overall, but one year at the most. Cited from: Werner E. Gerabek, Bernhard D. Haage, Gundolf Keil and Wolfgang Wegner: "Enzyklopädie der Medizingeschichte", Walter de Gruyter: Berlin, New York, 2007, p. 282. Note that these calculations are now viewed as likely even much less pronounced.)
A. Stewart Truswell: "Cholesterol and Beyond. The Research on Diet and Coronary Heart Disease 1900–2000", Springer: Dordrecht, Heidelberg, 2010, p. 158/9:
[citing: Dietary Prescription to Reduce the Risk of CHD from “ABC of Nutrition”, 3rd Edition (1999)  slightly outdated now, cited here for illustration of how outdated some advice to reduce dietary cholesterol is:]
Total fat. Reduction is not essential for improving plasma lipids but should reduce coagulation factors and day-time plasma
triglycerides and contribute to weight reduction.
Saturated fatty acids. Principally 14:0, 16:0 and 12:0 should be substantially reduced from around 15% of dietary energy in many
Western diets to 8–10%.
Polyunsaturated fatty acids. Mainly linoleic acid (18:2 ω-6): they should be about 7% of dietary energy (present British level), up to
10%. Omega-3 polyunsaturated fatty acids should be increased, both
20:5 and 22:6 from seafoods and 18:3 from canola (rapeseed) oil, etc.
Monounsaturated fatty acids. Ideal intake if total fat 30%, saturates
10% and polyunsaturated 8% would be 12% of total dietary energy.
Trans fatty acids. With the help of margarine manufacturers these are being reduced. The UK Department of Health recommends no more than
2% of dietary energy. Avoid older hard margarines.
Dietary cholesterol. This boils down to the question of egg yolks. Eggs are a nutritious, inexpensive and convenient food. The UK
Department of Health recommends for the general population no rise in
Salt (NaCl). Restriction to under 6.0 g/day is advised for the general popula- tion (100 mmol Na). It is more important for coronary
Fish. The UK Department of Health recommends at least twice a week, preferably fatty fish. It should not be fried in saturated fat.
Fibre. Oatmeal is recommended.
Vegetables and fruit. These are low in fat, and contain pectin and other fibres, flavonoids and other antioxidants, and they contain
folate. Expert Committees in Britain and the USA recommend five
servings of different vegetables and fruit per day (400 g/day average
Soy products (not salty soy sauce) recommended.
Alcohol in moderation, two to three drinks per day is beneficial for middle- aged people at risk of coronary heart disease but cannot be
recommended for the general population because of the greater danger
of accidents in younger people and of all the complications of
Coffee should be instant not filtered.
Even the very controversial researcher Ancel Keys had to reach this conclusion:
So Keys reached the counter-intuitive conclusion “there can be little doubt that, other things being equal, the serum cholesterol level is markedly influenced by the proportion of calories supplied by fats in the diet, that vegetable as well as animal fats have this effect, and that the dietary cholesterol itself is unimportant at all levels of intake practicable with natural foods.” [p. 14; original at Keys A (1952): "The cholesterol problem." Voeding, 13: 539–558.]
(Notice the date of this statement and that these conclusions about fat he drew were not unbiased but designed to promote carbohydrates.)
David Evans: "Cholesterol and Saturated Fat Prevent Heart Disease. Evidence from 101 Scientific Papers", Grosvenor House Publishing, Guildford, 2012. (Popular translation of and comments on selected papers, obviously biased but entertaining and not entirely incorrect.)
Frank P. Meyer: "Das Aus für die Cholesterol-Legende", BDI aktuell 11-2002, 14–19.
The International Network of Cholesterol Skeptics
Fabien De Meester, Sherma Zibadi and Ronald Ross Watson: "Modern Dietary Fat Intakes in Disease Promotion", Springer: New York, Dordrecht, 2010.